metadata: run_metadata: 20 rows where experiment.library_layout = "PAIRED", experiment.platform = "DNBSEQ" and tissue_curation

20 rows where experiment.library_layout = "PAIRED", experiment.platform = "DNBSEQ" and tissue_curation_coarse = "Cell Line"

descending

Link	rowid ▼	run.accession	experiment.accession	sample.accession	study.accession	bioproject	study.title	study.alias	study.type	study.abstract	sample.title	sample.alias	sample.attributes	GEOsample.title	GEOsample.dataprocessing	GEOsample.source	GEOsample.extractprotocol	GEOsample.characteristics	GEOsample.accession	experiment.title	experiment.alias	experiment.library_name	experiment.design_description	experiment.library_construction_protocol	experiment.library_strategy	experiment.library_source	experiment.library_selection	experiment.library_layout	experiment.platform	experiment.instrument_model	experiment.study_ref	run.filename	run.semantic_name	run.total_bases	run.total_spots	run.alias	run.read_lengths	run.base_counts	run.r1_length	run.r2_length	run.Acount	run.Ccount	run.Gcount	run.Tcount	run.experiment	run.pool_member	submission.accession	submission.srasource	submission.bioprojectsource	seqdetective.judgement.mate1	seqdetective.judgement.mate2	seqdetective.judgement.reason	platform_family	instrument_generation	read_bias	selection_class	prep_kit	sc_or_bulk	tech_class	technology	submission.bioprojectsource.country	earliest_date	devstage_curation	devstage_curation_coarse	tissue_curation	tissue_curation_coarse
32865	32865	SRR29488925	SRX24999628	SRS21700588	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	DKO5	GSM8343040	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO\|geo loc name:missing\|collection date:missing	DKO5	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO	GSM8343040	GSM8343040: DKO5; Danio rerio; RNA Seq	GSM8343040 r1	GSM8343040	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	DKO5_1.fq.gz DKO5_2.fq.gz	fastq fastq	4813408600.0	24067043.0	GSM8343040 r1	0:100 1:100	A:1302917202;C:1105312585;G:1123058369;T:1282120444;N:0	100	100	1302917202	1105312585	1123058369	1282120444	SRX24999628	SRS21700588	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32866	32866	SRR29488926	SRX24999627	SRS21700587	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	DKO4	GSM8343039	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO\|geo loc name:missing\|collection date:missing	DKO4	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO	GSM8343039	GSM8343039: DKO4; Danio rerio; RNA Seq	GSM8343039 r1	GSM8343039	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	DKO4_1.fq.gz DKO4_2.fq.gz	fastq fastq	4825860200.0	24129301.0	GSM8343039 r1	0:100 1:100	A:1303584214;C:1108617528;G:1131675283;T:1281983175;N:0	100	100	1303584214	1108617528	1131675283	1281983175	SRX24999627	SRS21700587	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32867	32867	SRR29488927	SRX24999626	SRS21700586	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	DKO3	GSM8343038	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO\|geo loc name:missing\|collection date:missing	DKO3	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO	GSM8343038	GSM8343038: DKO3; Danio rerio; RNA Seq	GSM8343038 r1	GSM8343038	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	DKO3_1.fq.gz DKO3_2.fq.gz	fastq fastq	4806754400.0	24033772.0	GSM8343038 r1	0:100 1:100	A:1289902978;C:1113397086;G:1131727783;T:1271726553;N:0	100	100	1289902978	1113397086	1131727783	1271726553	SRX24999626	SRS21700586	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32868	32868	SRR29488928	SRX24999625	SRS21700585	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	DKO2	GSM8343037	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO\|geo loc name:missing\|collection date:missing	DKO2	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO	GSM8343037	GSM8343037: DKO2; Danio rerio; RNA Seq	GSM8343037 r1	GSM8343037	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	DKO2_1.fq.gz DKO2_2.fq.gz	fastq fastq	4805757800.0	24028789.0	GSM8343037 r1	0:100 1:100	A:1299804990;C:1103101159;G:1124220106;T:1278631545;N:0	100	100	1299804990	1103101159	1124220106	1278631545	SRX24999625	SRS21700585	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32869	32869	SRR29488929	SRX24999624	SRS21700584	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	DKO1	GSM8343036	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO\|geo loc name:missing\|collection date:missing	DKO1	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:DKO	GSM8343036	GSM8343036: DKO1; Danio rerio; RNA Seq	GSM8343036 r1	GSM8343036	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	DKO1_1.fq.gz DKO1_2.fq.gz	fastq fastq	4819172400.0	24095862.0	GSM8343036 r1	0:100 1:100	A:1296017748;C:1112321357;G:1133115185;T:1277718110;N:0	100	100	1296017748	1112321357	1133115185	1277718110	SRX24999624	SRS21700584	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32870	32870	SRR29488930	SRX24999623	SRS21700583	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	GLO1KO5	GSM8343035	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO\|geo loc name:missing\|collection date:missing	GLO1KO5	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO	GSM8343035	GSM8343035: GLO1KO5; Danio rerio; RNA Seq	GSM8343035 r1	GSM8343035	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	GLO1KO5_1.fq.gz GLO1KO5_2.fq.gz	fastq fastq	4813614800.0	24068074.0	GSM8343035 r1	0:100 1:100	A:1289774342;C:1116099072;G:1136080400;T:1271660986;N:0	100	100	1289774342	1116099072	1136080400	1271660986	SRX24999623	SRS21700583	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32871	32871	SRR29488931	SRX24999622	SRS21700582	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	GLO1KO4	GSM8343034	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO\|geo loc name:missing\|collection date:missing	GLO1KO4	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO	GSM8343034	GSM8343034: GLO1KO4; Danio rerio; RNA Seq	GSM8343034 r1	GSM8343034	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	GLO1KO4_1.fq.gz GLO1KO4_2.fq.gz	fastq fastq	4805954200.0	24029771.0	GSM8343034 r1	0:100 1:100	A:1288997011;C:1113616764;G:1132409574;T:1270930851;N:0	100	100	1288997011	1113616764	1132409574	1270930851	SRX24999622	SRS21700582	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32872	32872	SRR29488932	SRX24999621	SRS21700581	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	GLO1KO3	GSM8343033	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO\|geo loc name:missing\|collection date:missing	GLO1KO3	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO	GSM8343033	GSM8343033: GLO1KO3; Danio rerio; RNA Seq	GSM8343033 r1	GSM8343033	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	GLO1KO3_1.fq.gz GLO1KO3_2.fq.gz	fastq fastq	4817965600.0	24089828.0	GSM8343033 r1	0:100 1:100	A:1290593290;C:1118086028;G:1134064137;T:1275222145;N:0	100	100	1290593290	1118086028	1134064137	1275222145	SRX24999621	SRS21700581	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32873	32873	SRR29488933	SRX24999620	SRS21700580	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	GLO1KO2	GSM8343032	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO\|geo loc name:missing\|collection date:missing	GLO1KO2	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO	GSM8343032	GSM8343032: GLO1KO2; Danio rerio; RNA Seq	GSM8343032 r1	GSM8343032	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	GLO1KO2_1.fq.gz GLO1KO2_2.fq.gz	fastq fastq	4805999000.0	24029995.0	GSM8343032 r1	0:100 1:100	A:1293609489;C:1109265811;G:1128786421;T:1274337279;N:0	100	100	1293609489	1109265811	1128786421	1274337279	SRX24999620	SRS21700580	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32874	32874	SRR29488934	SRX24999619	SRS21700579	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	GLO1KO1	GSM8343031	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO\|geo loc name:missing\|collection date:missing	GLO1KO1	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:GLO1KO	GSM8343031	GSM8343031: GLO1KO1; Danio rerio; RNA Seq	GSM8343031 r1	GSM8343031	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	GLO1KO1_1.fq.gz GLO1KO1_2.fq.gz	fastq fastq	4806768400.0	24033842.0	GSM8343031 r1	0:100 1:100	A:1286467027;C:1115478546;G:1135313631;T:1269509196;N:0	100	100	1286467027	1115478546	1135313631	1269509196	SRX24999619	SRS21700579	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32875	32875	SRR29488935	SRX24999618	SRS21700578	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	ALDH3A1KO5	GSM8343030	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO\|geo loc name:missing\|collection date:missing	ALDH3A1KO5	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO	GSM8343030	GSM8343030: ALDH3A1KO5; Danio rerio; RNA Seq	GSM8343030 r1	GSM8343030	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	ALDH3A1KO5_1.fq.gz ALDH3A1KO5_2.fq.gz	fastq fastq	4811331000.0	24056655.0	GSM8343030 r1	0:100 1:100	A:1314568654;C:1091419677;G:1111494171;T:1293848498;N:0	100	100	1314568654	1091419677	1111494171	1293848498	SRX24999618	SRS21700578	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32876	32876	SRR29488936	SRX24999617	SRS21700577	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	ALDH3A1KO4	GSM8343029	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO\|geo loc name:missing\|collection date:missing	ALDH3A1KO4	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO	GSM8343029	GSM8343029: ALDH3A1KO4; Danio rerio; RNA Seq	GSM8343029 r1	GSM8343029	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	ALDH3A1KO4_1.fq.gz ALDH3A1KO4_2.fq.gz	fastq fastq	4816993800.0	24084969.0	GSM8343029 r1	0:100 1:100	A:1320840277;C:1087361823;G:1108886472;T:1299905228;N:0	100	100	1320840277	1087361823	1108886472	1299905228	SRX24999617	SRS21700577	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32877	32877	SRR29488937	SRX24999616	SRS21700576	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	ALDH3A1KO3	GSM8343028	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO\|geo loc name:missing\|collection date:missing	ALDH3A1KO3	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO	GSM8343028	GSM8343028: ALDH3A1KO3; Danio rerio; RNA Seq	GSM8343028 r1	GSM8343028	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	ALDH3A1KO3_1.fq.gz ALDH3A1KO3_2.fq.gz	fastq fastq	4828261200.0	24141306.0	GSM8343028 r1	0:100 1:100	A:1325980327;C:1088988247;G:1107987702;T:1305304924;N:0	100	100	1325980327	1088988247	1107987702	1305304924	SRX24999616	SRS21700576	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32878	32878	SRR29488938	SRX24999615	SRS21700575	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	ALDH3A1KO2	GSM8343027	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO\|geo loc name:missing\|collection date:missing	ALDH3A1KO2	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO	GSM8343027	GSM8343027: ALDH3A1KO2; Danio rerio; RNA Seq	GSM8343027 r1	GSM8343027	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	ALDH3A1KO2_1.fq.gz ALDH3A1KO2_2.fq.gz	fastq fastq	4806790400.0	24033952.0	GSM8343027 r1	0:100 1:100	A:1296924744;C:1110667292;G:1117161162;T:1282037202;N:0	100	100	1296924744	1110667292	1117161162	1282037202	SRX24999615	SRS21700575	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32879	32879	SRR29488939	SRX24999614	SRS21700574	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	ALDH3A1KO1	GSM8343026	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO\|geo loc name:missing\|collection date:missing	ALDH3A1KO1	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:ALDH3A1KO	GSM8343026	GSM8343026: ALDH3A1KO1; Danio rerio; RNA Seq	GSM8343026 r1	GSM8343026	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	ALDH3A1KO1_1.fq.gz ALDH3A1KO1_2.fq.gz	fastq fastq	4801013600.0	24005068.0	GSM8343026 r1	0:100 1:100	A:1307355551;C:1094613295;G:1111765622;T:1287279132;N:0	100	100	1307355551	1094613295	1111765622	1287279132	SRX24999614	SRS21700574	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32880	32880	SRR29488940	SRX24999613	SRS21700573	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	WT5	GSM8343025	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT\|geo loc name:missing\|collection date:missing	WT5	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT	GSM8343025	GSM8343025: WT5; Danio rerio; RNA Seq	GSM8343025 r1	GSM8343025	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	WT5_1.fq.gz WT5_2.fq.gz	fastq fastq	4820580400.0	24102902.0	GSM8343025 r1	0:100 1:100	A:1288306977;C:1120287477;G:1138943028;T:1273042918;N:0	100	100	1288306977	1120287477	1138943028	1273042918	SRX24999613	SRS21700573	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32881	32881	SRR29488941	SRX24999612	SRS21700572	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	WT4	GSM8343024	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT\|geo loc name:missing\|collection date:missing	WT4	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT	GSM8343024	GSM8343024: WT4; Danio rerio; RNA Seq	GSM8343024 r1	GSM8343024	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	WT4_1.fq.gz WT4_2.fq.gz	fastq fastq	4821144600.0	24105723.0	GSM8343024 r1	0:100 1:100	A:1275218149;C:1133748961;G:1151831603;T:1260345887;N:0	100	100	1275218149	1133748961	1151831603	1260345887	SRX24999612	SRS21700572	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32882	32882	SRR29488942	SRX24999611	SRS21700571	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	WT3	GSM8343023	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT\|geo loc name:missing\|collection date:missing	WT3	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT	GSM8343023	GSM8343023: WT3; Danio rerio; RNA Seq	GSM8343023 r1	GSM8343023	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	WT3_1.fq.gz WT3_2.fq.gz	fastq fastq	4826072600.0	24130363.0	GSM8343023 r1	0:100 1:100	A:1278424901;C:1132200743;G:1150406212;T:1265040744;N:0	100	100	1278424901	1132200743	1150406212	1265040744	SRX24999611	SRS21700571	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32883	32883	SRR29488943	SRX24999610	SRS21700570	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	WT2	GSM8343022	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT\|geo loc name:missing\|collection date:missing	WT2	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT	GSM8343022	GSM8343022: WT2; Danio rerio; RNA Seq	GSM8343022 r1	GSM8343022	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	WT2_1.fq.gz WT2_2.fq.gz	fastq fastq	4801181000.0	24005905.0	GSM8343022 r1	0:100 1:100	A:1271169177;C:1127438892;G:1145437659;T:1257135272;N:0	100	100	1271169177	1127438892	1145437659	1257135272	SRX24999610	SRS21700570	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line
32884	32884	SRR29488944	SRX24999609	SRS21700569	SRP515253	PRJNA1126644	Elevated MG H1 in glo1 / aldh3a1 / zebrafish caused microvasculature alterations and glucose metabolism impairment via decreased proteasome activity	GSE270442	Transcriptome Analysis	Dicarbonyl stress is characterized by the abnormal accumulation of dicarbonyl reactive metabolites leading to increased modification of proteins DNA and lipids thereby contributing to cellular and tissue dysfunction in diabetes diabetic complications and other diseases. glo1 knockout zebrafish exhibited moderately increased MG levels yet this was inadequate to induce trunk vessels alterations due to elevated ALDH activity and mRNA expression levels which partially act as compensatory mechanism. Excess 4 HNE induced pancreas dysfunction in aldh3a1 knockout zebrafish larvae inhibiting insulin expression and thereby facilitating hyperglycemia and hyaloid vasculature alterations. To evaluate the combined function of Glo1 and Aldh3a1 in glucose homeostasis and diabetic microvasculature glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish. glo1 / aldh3a1 / zebrafish larvae displayed angiogenic hyaloid vasculature caused by the elevated MG H1 and decreased proteasomal chymotrypsin like activity which could be rescued by the MG H1 scavenger L carnosine and proteasome activator Betulinic acid treatments. In adult glo1 / aldh3a1 / zebrafish impaired glucose metabolism angiogenic retina vasculature and thickened GBM were observed. Thus our data suggested that an important upstream factor contributing to these phenomena in the context of lacking glo1 and aldh3a1 is MG H1 possibly through reduced proteasome activity. Overall design: glo1 / aldh3a1 / zebrafish were generated using CRISPR/Cas9 technology. Multiple experiments are performed regarding vasculature alterations glucose homeostasis transcriptome and metabolomics in Tgfli1:EGFP zebrafish.	WT1	GSM8343021	source name:larvae\|tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT\|geo loc name:missing\|collection date:missing	WT1	Raw sequence data with adapter sequences or low quality sequences was filtered. Filtered reads were aligned to the Zebrafish reference genome GRCz11 Raw counts levels were quantified using FeatureCounts v2.0.3 Assembly: GRCz11 Supplementary files format and content: tab delimited text file includes raw counts for each sample.	larvae	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	tissue:larvae\|cell line:Tgfli1:EGFP\|cell type:larvae\|genotype:WT	GSM8343021	GSM8343021: WT1; Danio rerio; RNA Seq	GSM8343021 r1	GSM8343021	1	Total RNA was extracted using RNeasy Mini KitQIAGEN 3ug of total RNA was used for the construction of sequencing libraries. RNA libraries for RNA seq were prepared using DNBSEQ Eukaryotic Strand specific mRNA library.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	DNBSEQ	DNBSEQ-G400	SRP515253	WT1_1.fq.gz WT1_2.fq.gz	fastq fastq	4802502800.0	24012514.0	GSM8343021 r1	0:100 1:100	A:1263416018;C:1135581393;G:1152700487;T:1250804902;N:0	100	100	1263416018	1135581393	1152700487	1250804902	SRX24999609	SRS21700569	SRA1904686	ECAS	ECAS	B	B	biological fallback assumption	bgi	bgi	unknown	cdna_unspecified	unknown	bulk	unknown	unknown	Unknown	2024-06-21	Larval	Larval	Cell Line	Cell Line

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CREATE TABLE run_metadata("run.accession" VARCHAR, "experiment.accession" VARCHAR, "sample.accession" VARCHAR, "study.accession" VARCHAR, bioproject VARCHAR, "study.title" VARCHAR, "study.alias" VARCHAR, "study.type" VARCHAR, "study.abstract" VARCHAR, "study.attributes" VARCHAR, "study.PMIDs" VARCHAR, "sample.description" VARCHAR, "sample.title" VARCHAR, "sample.alias" VARCHAR, "sample.centername" VARCHAR, "sample.attributes" VARCHAR, "GEOsample.title" VARCHAR, "GEOsample.dataprocessing" VARCHAR, "GEOsample.source" VARCHAR, "GEOsample.treatmentprotocol" VARCHAR, "GEOsample.extractprotocol" VARCHAR, "GEOsample.growthprotocol" VARCHAR, "GEOsample.characteristics" VARCHAR, "GEOsample.accession" VARCHAR, "experiment.title" VARCHAR, "experiment.alias" VARCHAR, "experiment.library_name" VARCHAR, "experiment.design_description" VARCHAR, "experiment.library_construction_protocol" VARCHAR, "experiment.attributes" VARCHAR, "experiment.library_strategy" VARCHAR, "experiment.library_source" VARCHAR, "experiment.library_selection" VARCHAR, "experiment.library_layout" VARCHAR, "experiment.platform" VARCHAR, "experiment.instrument_model" VARCHAR, "experiment.spot_descriptor" VARCHAR, "experiment.study_ref" VARCHAR, "run.title" VARCHAR, "run.attributes" VARCHAR, "run.filename" VARCHAR, "run.semantic_name" VARCHAR, "run.total_bases" DOUBLE, "run.total_spots" DOUBLE, "run.alias" VARCHAR, "run.read_lengths" VARCHAR, "run.base_counts" VARCHAR, "run.r1_length" BIGINT, "run.r2_length" BIGINT, "run.r3_length" BIGINT, "run.r4_length" BIGINT, "run.Acount" BIGINT, "run.Ccount" BIGINT, "run.Gcount" BIGINT, "run.Tcount" BIGINT, "run.Ncount" BIGINT, "run.experiment" VARCHAR, "run.pool_member" VARCHAR, "submission.accession" VARCHAR, "submission.srasource" VARCHAR, "submission.bioprojectsource" VARCHAR, "seqdetective.n_mates" BIGINT, "seqdetective.mapping_rate.mate1" DOUBLE, "seqdetective.mapping_rate.mate2" DOUBLE, "seqdetective.nofeature_rate.mate1" DOUBLE, "seqdetective.nofeature_rate.mate2" DOUBLE, "seqdetective.sparsity.mate1" DOUBLE, "seqdetective.sparsity.mate2" DOUBLE, "seqdetective.pos_strand_rate.mate1" DOUBLE, "seqdetective.pos_strand_rate.mate2" DOUBLE, "seqdetective.readlen.mate1" BIGINT, "seqdetective.readlen.mate2" BIGINT, "seqdetective.judgement.mate1" VARCHAR, "seqdetective.judgement.mate2" VARCHAR, "seqdetective.judgement.reason" VARCHAR, platform_family VARCHAR, instrument_generation VARCHAR, read_bias VARCHAR, selection_class VARCHAR, prep_kit VARCHAR, sc_or_bulk VARCHAR, tech_class VARCHAR, technology VARCHAR, tech_variant VARCHAR, "submission.bioprojectsource.country" VARCHAR, earliest_date DATE, devstage_curation VARCHAR, devstage_curation_coarse VARCHAR, tissue_curation VARCHAR, tissue_curation_coarse VARCHAR);;
CREATE INDEX idx_run_bioproject ON run_metadata(bioproject);;
CREATE INDEX idx_run_run_accession ON run_metadata("run.accession");;