run_metadata
4 rows where experiment.library_source = "TRANSCRIPTOMIC", technology = "celseq" and tissue_curation = "Liver"
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| Link | rowid ▼ | run.accession | experiment.accession | sample.accession | study.accession | bioproject | study.title | study.alias | study.type | study.abstract | study.attributes | study.PMIDs | sample.description | sample.title | sample.alias | sample.centername | sample.attributes | GEOsample.title | GEOsample.dataprocessing | GEOsample.source | GEOsample.treatmentprotocol | GEOsample.extractprotocol | GEOsample.growthprotocol | GEOsample.characteristics | GEOsample.accession | experiment.title | experiment.alias | experiment.library_name | experiment.design_description | experiment.library_construction_protocol | experiment.attributes | experiment.library_strategy | experiment.library_source | experiment.library_selection | experiment.library_layout | experiment.platform | experiment.instrument_model | experiment.spot_descriptor | experiment.study_ref | run.title | run.attributes | 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.r3_length | run.r4_length | run.Acount | run.Ccount | run.Gcount | run.Tcount | run.Ncount | run.experiment | run.pool_member | submission.accession | submission.srasource | submission.bioprojectsource | seqdetective.n_mates | seqdetective.mapping_rate.mate1 | seqdetective.mapping_rate.mate2 | seqdetective.nofeature_rate.mate1 | seqdetective.nofeature_rate.mate2 | seqdetective.sparsity.mate1 | seqdetective.sparsity.mate2 | seqdetective.pos_strand_rate.mate1 | seqdetective.pos_strand_rate.mate2 | seqdetective.readlen.mate1 | seqdetective.readlen.mate2 | 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 | tech_variant | submission.bioprojectsource.country | earliest_date | devstage_curation | devstage_curation_coarse | tissue_curation | tissue_curation_coarse |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 70094 | 70094 | SRR19520282 | SRX15572798 | SRS13275626 | SRP378140 | PRJNA844556 | Loss of pex5 sensitizes zebrafish to fasting due to deregulated mitochondria mTOR and autophagy | GSE205349 | Transcriptome Analysis | Animal models have been utilized to understand the pathogenesis of Zellweger spectrum disorders ZSD but the link between the clinical manifestations and molecular pathways has not yet been clearly established. We generated a peroxin 5 homozygous mutant zebrafish pex5 / to gain insight into the molecular pathogenesis of peroxisome dysfunction. pex5 / displays hallmarks of ZSD in humans and die within one month post birth. Fasting rapidly depletes the liver lipids and glycogen in pex5 / and expedites their mortality. Mechanistically abnormal mitochondrial activity and mechanistic target of rapamycin mTOR signaling act together to induce metabolic alterations to deplete the hepatic nutrients and accumulate the damaged mitochondria. Accordingly the use of chemical interventions blocking either the mitochondrial activities or the mechanistic target of rapamycin complex 1 or a combination of both improves the metabolic imbalance shown in the fasted pex5 / livers and extends the survival of the animals. Furthermore the use of an autophagy activator also effectively ameliorated the early mortality of the fasted pex5 / . These results suggest that fasting may be detrimental to patients with peroxisome dysfunction and that modulating the mitochondria mTOR or autophagy activities may provide a therapeutic option to alleviate the symptoms of peroxisomal diseases associated with metabolic dysfunction. Overall design: Total RNAs of whole liver tissues from fasted WT and pex5 homozygous mutant zebrafish at 6 dpf were used to identify differential gene expression between the two genotype under fasting condition | pubmed:36821008 | pex5KO 6dpf 2 [N047 06] | GSM6210777 | source name:liver|tissue:liver|genotype:pex5 KO|treatment:fasted | pex5KO 6dpf 2 [N047 06] | Quantitative analysis was performed using 51bp of insert reads Read2. Cell barcode and UMI in Read1 was extracted by using UMI tools ver.1.1.1. Four cell barcodes were mixed and used for all samples. Adaptor sequence and low quality sequence were removed and read length below 20bp were discarded by using Trim Galore ver.0.6.7. Reads were mapped to the GRCz11 reference using HISAT2 ver.2.2.1. Read counts for each gene were obtained by featureCounts ver.2.0.1. UMI duplication was removed by UMI tools. Assembly: GRCz11 Supplementary files format and content: tab delimited text files include TMM values for each Sample | liver | Total RNA was extracted by using Direct zol RNA Kit ZYMO RESEARCH according to the manufacture’s instruction. 3’UTR RNA seq was performed using the CEL Seq2 protocol except that Second Strand Synthesis Module NEB was used for double stranded cDNA synthesis and library was amplified by 9 cycles of PCR without xxx sample pooling. | tissue:liver|genotype:pex5 KO|treatment:fasted | GSM6210777 | GSM6210777: pex5KO 6dpf 2 [N047 06]; Danio rerio; RNA Seq | GSM6210777 r1 | GSM6210777 | 1 | Total RNA was extracted by using Direct zol RNA Kit ZYMO RESEARCH according to the manufacture's instruction. three primeUTR RNA seq was performed using the CEL Seq2 protocol except that Second Strand Synthesis Module NEB was used for double stranded cDNA synthesis and library was amplified by 9 cycles of PCR without xxx sample pooling. | RNA-Seq | TRANSCRIPTOMIC | cDNA | PAIRED | ILLUMINA | Illumina MiniSeq | SRP378140 | N047-06_S6_L001_R1_001.fastq.gz N047-06_S6_L001_R2_001.fastq.gz | fastq fastq | 174282570.0 | 2489751.0 | GSM6210777 r1 | 0:19 1:51 | A:44582662;C:35509006;G:39346826;T:54785033;N:59043 | 19 | 51 | 44582662 | 35509006 | 39346826 | 54785033 | 59043 | SRX15572798 | SRS13275626 | SRA1430748 | Sungkyunkwan University | Sungkyunkwan University | 2 | 0.01246 | 0.9141 | 0.01046 | 0.0952 | 0.99391 | 0.84159 | 0.53989 | 0.66354 | 19 | 51 | T | B | sc-like readlen | illumina | miseq | unknown | cdna_unspecified | unknown | sc | single_cell_plate | celseq | South Korea | 2022-06-02 | Larval | Larval | Liver | Liver and Biliary System | ||||||||||||
| 70095 | 70095 | SRR19520283 | SRX15572797 | SRS13275623 | SRP378140 | PRJNA844556 | Loss of pex5 sensitizes zebrafish to fasting due to deregulated mitochondria mTOR and autophagy | GSE205349 | Transcriptome Analysis | Animal models have been utilized to understand the pathogenesis of Zellweger spectrum disorders ZSD but the link between the clinical manifestations and molecular pathways has not yet been clearly established. We generated a peroxin 5 homozygous mutant zebrafish pex5 / to gain insight into the molecular pathogenesis of peroxisome dysfunction. pex5 / displays hallmarks of ZSD in humans and die within one month post birth. Fasting rapidly depletes the liver lipids and glycogen in pex5 / and expedites their mortality. Mechanistically abnormal mitochondrial activity and mechanistic target of rapamycin mTOR signaling act together to induce metabolic alterations to deplete the hepatic nutrients and accumulate the damaged mitochondria. Accordingly the use of chemical interventions blocking either the mitochondrial activities or the mechanistic target of rapamycin complex 1 or a combination of both improves the metabolic imbalance shown in the fasted pex5 / livers and extends the survival of the animals. Furthermore the use of an autophagy activator also effectively ameliorated the early mortality of the fasted pex5 / . These results suggest that fasting may be detrimental to patients with peroxisome dysfunction and that modulating the mitochondria mTOR or autophagy activities may provide a therapeutic option to alleviate the symptoms of peroxisomal diseases associated with metabolic dysfunction. Overall design: Total RNAs of whole liver tissues from fasted WT and pex5 homozygous mutant zebrafish at 6 dpf were used to identify differential gene expression between the two genotype under fasting condition | pubmed:36821008 | pex5KO 6dpf 1 [N047 05] | GSM6210776 | source name:liver|tissue:liver|genotype:pex5 KO|treatment:fasted | pex5KO 6dpf 1 [N047 05] | Quantitative analysis was performed using 51bp of insert reads Read2. Cell barcode and UMI in Read1 was extracted by using UMI tools ver.1.1.1. Four cell barcodes were mixed and used for all samples. Adaptor sequence and low quality sequence were removed and read length below 20bp were discarded by using Trim Galore ver.0.6.7. Reads were mapped to the GRCz11 reference using HISAT2 ver.2.2.1. Read counts for each gene were obtained by featureCounts ver.2.0.1. UMI duplication was removed by UMI tools. Assembly: GRCz11 Supplementary files format and content: tab delimited text files include TMM values for each Sample | liver | Total RNA was extracted by using Direct zol RNA Kit ZYMO RESEARCH according to the manufacture’s instruction. 3’UTR RNA seq was performed using the CEL Seq2 protocol except that Second Strand Synthesis Module NEB was used for double stranded cDNA synthesis and library was amplified by 9 cycles of PCR without xxx sample pooling. | tissue:liver|genotype:pex5 KO|treatment:fasted | GSM6210776 | GSM6210776: pex5KO 6dpf 1 [N047 05]; Danio rerio; RNA Seq | GSM6210776 r1 | GSM6210776 | 1 | Total RNA was extracted by using Direct zol RNA Kit ZYMO RESEARCH according to the manufacture's instruction. three primeUTR RNA seq was performed using the CEL Seq2 protocol except that Second Strand Synthesis Module NEB was used for double stranded cDNA synthesis and library was amplified by 9 cycles of PCR without xxx sample pooling. | RNA-Seq | TRANSCRIPTOMIC | cDNA | PAIRED | ILLUMINA | Illumina MiniSeq | SRP378140 | N047-05_S5_L001_R1_001.fastq.gz N047-05_S5_L001_R2_001.fastq.gz | fastq fastq | 172133920.0 | 2459056.0 | GSM6210776 r1 | 0:19 1:51 | A:45030545;C:35152439;G:38626479;T:53266372;N:58085 | 19 | 51 | 45030545 | 35152439 | 38626479 | 53266372 | 58085 | SRX15572797 | SRS13275623 | SRA1430748 | Sungkyunkwan University | Sungkyunkwan University | 2 | 0.01077 | 0.9045 | 0.00913 | 0.08354 | 0.99498 | 0.85535 | 0.55921 | 0.67705 | 19 | 51 | T | B | sc-like readlen | illumina | miseq | unknown | cdna_unspecified | unknown | sc | single_cell_plate | celseq | South Korea | 2022-06-02 | Larval | Larval | Liver | Liver and Biliary System | ||||||||||||
| 70096 | 70096 | SRR19520284 | SRX15572796 | SRS13275624 | SRP378140 | PRJNA844556 | Loss of pex5 sensitizes zebrafish to fasting due to deregulated mitochondria mTOR and autophagy | GSE205349 | Transcriptome Analysis | Animal models have been utilized to understand the pathogenesis of Zellweger spectrum disorders ZSD but the link between the clinical manifestations and molecular pathways has not yet been clearly established. We generated a peroxin 5 homozygous mutant zebrafish pex5 / to gain insight into the molecular pathogenesis of peroxisome dysfunction. pex5 / displays hallmarks of ZSD in humans and die within one month post birth. Fasting rapidly depletes the liver lipids and glycogen in pex5 / and expedites their mortality. Mechanistically abnormal mitochondrial activity and mechanistic target of rapamycin mTOR signaling act together to induce metabolic alterations to deplete the hepatic nutrients and accumulate the damaged mitochondria. Accordingly the use of chemical interventions blocking either the mitochondrial activities or the mechanistic target of rapamycin complex 1 or a combination of both improves the metabolic imbalance shown in the fasted pex5 / livers and extends the survival of the animals. Furthermore the use of an autophagy activator also effectively ameliorated the early mortality of the fasted pex5 / . These results suggest that fasting may be detrimental to patients with peroxisome dysfunction and that modulating the mitochondria mTOR or autophagy activities may provide a therapeutic option to alleviate the symptoms of peroxisomal diseases associated with metabolic dysfunction. Overall design: Total RNAs of whole liver tissues from fasted WT and pex5 homozygous mutant zebrafish at 6 dpf were used to identify differential gene expression between the two genotype under fasting condition | pubmed:36821008 | WT 6dpf 4 [N047 04] | GSM6210775 | source name:liver|tissue:liver|genotype:Wild type|treatment:fasted | WT 6dpf 4 [N047 04] | Quantitative analysis was performed using 51bp of insert reads Read2. Cell barcode and UMI in Read1 was extracted by using UMI tools ver.1.1.1. Four cell barcodes were mixed and used for all samples. Adaptor sequence and low quality sequence were removed and read length below 20bp were discarded by using Trim Galore ver.0.6.7. Reads were mapped to the GRCz11 reference using HISAT2 ver.2.2.1. Read counts for each gene were obtained by featureCounts ver.2.0.1. UMI duplication was removed by UMI tools. Assembly: GRCz11 Supplementary files format and content: tab delimited text files include TMM values for each Sample | liver | Total RNA was extracted by using Direct zol RNA Kit ZYMO RESEARCH according to the manufacture’s instruction. 3’UTR RNA seq was performed using the CEL Seq2 protocol except that Second Strand Synthesis Module NEB was used for double stranded cDNA synthesis and library was amplified by 9 cycles of PCR without xxx sample pooling. | tissue:liver|genotype:Wild type|treatment:fasted | GSM6210775 | GSM6210775: WT 6dpf 4 [N047 04]; Danio rerio; RNA Seq | GSM6210775 r1 | GSM6210775 | 1 | Total RNA was extracted by using Direct zol RNA Kit ZYMO RESEARCH according to the manufacture's instruction. three primeUTR RNA seq was performed using the CEL Seq2 protocol except that Second Strand Synthesis Module NEB was used for double stranded cDNA synthesis and library was amplified by 9 cycles of PCR without xxx sample pooling. | RNA-Seq | TRANSCRIPTOMIC | cDNA | PAIRED | ILLUMINA | Illumina MiniSeq | SRP378140 | N047-04_S4_L001_R1_001.fastq.gz N047-04_S4_L001_R2_001.fastq.gz | fastq fastq | 147083090.0 | 2101187.0 | GSM6210775 r1 | 0:19 1:51 | A:37975239;C:30348934;G:33184532;T:45523625;N:50760 | 19 | 51 | 37975239 | 30348934 | 33184532 | 45523625 | 50760 | SRX15572796 | SRS13275624 | SRA1430748 | Sungkyunkwan University | Sungkyunkwan University | 2 | 0.01149 | 0.91123 | 0.00998 | 0.0933 | 0.99515 | 0.84928 | 0.51408 | 0.66541 | 19 | 51 | T | B | sc-like readlen | illumina | miseq | unknown | cdna_unspecified | unknown | sc | single_cell_plate | celseq | South Korea | 2022-06-02 | Larval | Larval | Liver | Liver and Biliary System | ||||||||||||
| 70097 | 70097 | SRR19520285 | SRX15572795 | SRS13275625 | SRP378140 | PRJNA844556 | Loss of pex5 sensitizes zebrafish to fasting due to deregulated mitochondria mTOR and autophagy | GSE205349 | Transcriptome Analysis | Animal models have been utilized to understand the pathogenesis of Zellweger spectrum disorders ZSD but the link between the clinical manifestations and molecular pathways has not yet been clearly established. We generated a peroxin 5 homozygous mutant zebrafish pex5 / to gain insight into the molecular pathogenesis of peroxisome dysfunction. pex5 / displays hallmarks of ZSD in humans and die within one month post birth. Fasting rapidly depletes the liver lipids and glycogen in pex5 / and expedites their mortality. Mechanistically abnormal mitochondrial activity and mechanistic target of rapamycin mTOR signaling act together to induce metabolic alterations to deplete the hepatic nutrients and accumulate the damaged mitochondria. Accordingly the use of chemical interventions blocking either the mitochondrial activities or the mechanistic target of rapamycin complex 1 or a combination of both improves the metabolic imbalance shown in the fasted pex5 / livers and extends the survival of the animals. Furthermore the use of an autophagy activator also effectively ameliorated the early mortality of the fasted pex5 / . These results suggest that fasting may be detrimental to patients with peroxisome dysfunction and that modulating the mitochondria mTOR or autophagy activities may provide a therapeutic option to alleviate the symptoms of peroxisomal diseases associated with metabolic dysfunction. Overall design: Total RNAs of whole liver tissues from fasted WT and pex5 homozygous mutant zebrafish at 6 dpf were used to identify differential gene expression between the two genotype under fasting condition | pubmed:36821008 | WT 6dpf 1 [N047 01] | GSM6210774 | source name:liver|tissue:liver|genotype:Wild type|treatment:fasted | WT 6dpf 1 [N047 01] | Quantitative analysis was performed using 51bp of insert reads Read2. Cell barcode and UMI in Read1 was extracted by using UMI tools ver.1.1.1. Four cell barcodes were mixed and used for all samples. Adaptor sequence and low quality sequence were removed and read length below 20bp were discarded by using Trim Galore ver.0.6.7. Reads were mapped to the GRCz11 reference using HISAT2 ver.2.2.1. Read counts for each gene were obtained by featureCounts ver.2.0.1. UMI duplication was removed by UMI tools. Assembly: GRCz11 Supplementary files format and content: tab delimited text files include TMM values for each Sample | liver | Total RNA was extracted by using Direct zol RNA Kit ZYMO RESEARCH according to the manufacture’s instruction. 3’UTR RNA seq was performed using the CEL Seq2 protocol except that Second Strand Synthesis Module NEB was used for double stranded cDNA synthesis and library was amplified by 9 cycles of PCR without xxx sample pooling. | tissue:liver|genotype:Wild type|treatment:fasted | GSM6210774 | GSM6210774: WT 6dpf 1 [N047 01]; Danio rerio; RNA Seq | GSM6210774 r1 | GSM6210774 | 1 | Total RNA was extracted by using Direct zol RNA Kit ZYMO RESEARCH according to the manufacture's instruction. three primeUTR RNA seq was performed using the CEL Seq2 protocol except that Second Strand Synthesis Module NEB was used for double stranded cDNA synthesis and library was amplified by 9 cycles of PCR without xxx sample pooling. | RNA-Seq | TRANSCRIPTOMIC | cDNA | PAIRED | ILLUMINA | Illumina MiniSeq | SRP378140 | N047-01_S1_L001_R1_001.fastq.gz N047-01_S1_L001_R2_001.fastq.gz | fastq fastq | 174019160.0 | 2485988.0 | GSM6210774 r1 | 0:19 1:51 | A:44401044;C:36220148;G:39239552;T:54096960;N:61456 | 19 | 51 | 44401044 | 36220148 | 39239552 | 54096960 | 61456 | SRX15572795 | SRS13275625 | SRA1430748 | Sungkyunkwan University | Sungkyunkwan University | 2 | 0.01132 | 0.90822 | 0.00976 | 0.09386 | 0.99504 | 0.84118 | 0.54452 | 0.66722 | 19 | 51 | T | B | sc-like readlen | illumina | miseq | unknown | cdna_unspecified | unknown | sc | single_cell_plate | celseq | South Korea | 2022-06-02 | Larval | Larval | Liver | Liver and Biliary System |
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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");;