{"database": "metadata", "table": "run_metadata", "is_view": false, "human_description_en": "where experiment.library_selection = \"PolyA\", technology = \"unknown\" and tissue_curation_coarse = \"Cardiovascular System\"", "rows": [[31715, "SRR28508805", "SRX24109965", "SRS20897113", "SRP498846", "PRJNA1094457", "Danio rerio Transcriptome or Gene expression", "PRJNA1094457", "Other", "Atrial cardiomyopathy  which often comes with underlying genetic defects  has been recognized as a possible substrate of atrial fibrillation. MYH6 encodes a myosin heavy chain a MHC  predominantly expressed in the atria and pivotal in sarcomere organization and muscle contraction. However  the role of MYH6 in atrial diseases has not been fully elucidated and the genetic cause of atrial cardiomyopathy needs further investigation. Here  we employed CRISPR/Cas9 to generate myh6 knockout zebrafish  assessing cardiac function through diverse methodologies  including video analysis  ECG  echocardiography  transmission electron microscopy  and transcriptomic sequencing. Our findings revealed that myh6 defects in zebrafish led to impaired atrial and ventricular function and disordered sarcomere. This research underscores the pivotal role of MYH6 in maintaining atrial function and development. The observed connections between sarcomeric gene variants and atrial cardiomyopathy contribute to our understanding of the genetic basis of atrial fibrillation.", null, null, null, "myh6+/  3", "Sample 6", null, "strain:not collected|isolate:not collected|breed:not collected|cultivar:not collected|ecotype:not collected|age:6 mpf|dev stage:not collected|collection date:2023 09 03|geo loc name:not collected|sex:pooled male and female|tissue:heart|genotype:myh6+/ |BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "myh6+/  3", "Sample 6", "Sample 6", "Sequencing data were analyzed by R studio Version 2023.03.0+386. Differentially expressed genes DEGs between the experimental myh6+/  and control wildtype groups were identified using the DESeq2 package.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP498846", null, null, "7_230906N_S64_L004_R1_001.fastq.gz 7_230906N_S64_L004_R2_001.fastq.gz", "fastq fastq", 5096818364.0, 16876882.0, "7 230906N S64 L004 R1 001.fastq.gz", "0:151 1:151", "A:1417476599;C:1123713516;G:1180970526;T:1374564888;N:92835", 151, 151, null, null, 1417476599, 1123713516, 1180970526, 1374564888, 92835, "SRX24109965", "SRS20897113", "SRA1836610", "Nanjing medical university|Cardiology", "Nanjing medical university", 2, 0.92843, 0.93025, 0.09825, 0.0937, 0.7601, 0.76081, 0.46245, 0.45548, 151, 151, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "China", "2024-03-31", "Adult", "Adult", "Heart", "Cardiovascular System"], [31716, "SRR28508806", "SRX24109964", "SRS20897112", "SRP498846", "PRJNA1094457", "Danio rerio Transcriptome or Gene expression", "PRJNA1094457", "Other", "Atrial cardiomyopathy  which often comes with underlying genetic defects  has been recognized as a possible substrate of atrial fibrillation. MYH6 encodes a myosin heavy chain a MHC  predominantly expressed in the atria and pivotal in sarcomere organization and muscle contraction. However  the role of MYH6 in atrial diseases has not been fully elucidated and the genetic cause of atrial cardiomyopathy needs further investigation. Here  we employed CRISPR/Cas9 to generate myh6 knockout zebrafish  assessing cardiac function through diverse methodologies  including video analysis  ECG  echocardiography  transmission electron microscopy  and transcriptomic sequencing. Our findings revealed that myh6 defects in zebrafish led to impaired atrial and ventricular function and disordered sarcomere. This research underscores the pivotal role of MYH6 in maintaining atrial function and development. The observed connections between sarcomeric gene variants and atrial cardiomyopathy contribute to our understanding of the genetic basis of atrial fibrillation.", null, null, null, "myh6+/  2", "Sample 5", null, "strain:not collected|isolate:not collected|breed:not collected|cultivar:not collected|ecotype:not collected|age:6 mpf|dev stage:not collected|collection date:2023 09 03|geo loc name:not collected|sex:pooled male and female|tissue:heart|genotype:myh6+/ |BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "myh6+/  2", "Sample 5", "Sample 5", "Sequencing data were analyzed by R studio Version 2023.03.0+386. 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MYH6 encodes a myosin heavy chain a MHC  predominantly expressed in the atria and pivotal in sarcomere organization and muscle contraction. However  the role of MYH6 in atrial diseases has not been fully elucidated and the genetic cause of atrial cardiomyopathy needs further investigation. Here  we employed CRISPR/Cas9 to generate myh6 knockout zebrafish  assessing cardiac function through diverse methodologies  including video analysis  ECG  echocardiography  transmission electron microscopy  and transcriptomic sequencing. Our findings revealed that myh6 defects in zebrafish led to impaired atrial and ventricular function and disordered sarcomere. This research underscores the pivotal role of MYH6 in maintaining atrial function and development. The observed connections between sarcomeric gene variants and atrial cardiomyopathy contribute to our understanding of the genetic basis of atrial fibrillation.", null, null, null, "myh6+/  1", "Sample 4", null, "strain:not collected|isolate:not collected|breed:not collected|cultivar:not collected|ecotype:not collected|age:6 mpf|dev stage:not collected|collection date:2023 09 03|geo loc name:not collected|sex:pooled male and female|tissue:heart|genotype:myh6+/ |BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "myh6+/  1", "Sample 4", "Sample 4", "Sequencing data were analyzed by R studio Version 2023.03.0+386. 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MYH6 encodes a myosin heavy chain a MHC  predominantly expressed in the atria and pivotal in sarcomere organization and muscle contraction. However  the role of MYH6 in atrial diseases has not been fully elucidated and the genetic cause of atrial cardiomyopathy needs further investigation. Here  we employed CRISPR/Cas9 to generate myh6 knockout zebrafish  assessing cardiac function through diverse methodologies  including video analysis  ECG  echocardiography  transmission electron microscopy  and transcriptomic sequencing. Our findings revealed that myh6 defects in zebrafish led to impaired atrial and ventricular function and disordered sarcomere. This research underscores the pivotal role of MYH6 in maintaining atrial function and development. The observed connections between sarcomeric gene variants and atrial cardiomyopathy contribute to our understanding of the genetic basis of atrial fibrillation.", null, null, null, "WT 3", "Sample 3", null, "strain:not collected|isolate:not collected|breed:not collected|cultivar:not collected|ecotype:not collected|age:6 mpf|dev stage:not collected|collection date:2023 09 03|geo loc name:not collected|sex:pooled male and female|tissue:heart|genotype:wild type|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "WT 3", "Sample 3", "Sample 3", "Sequencing data were analyzed by R studio Version 2023.03.0+386. 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MYH6 encodes a myosin heavy chain a MHC  predominantly expressed in the atria and pivotal in sarcomere organization and muscle contraction. However  the role of MYH6 in atrial diseases has not been fully elucidated and the genetic cause of atrial cardiomyopathy needs further investigation. Here  we employed CRISPR/Cas9 to generate myh6 knockout zebrafish  assessing cardiac function through diverse methodologies  including video analysis  ECG  echocardiography  transmission electron microscopy  and transcriptomic sequencing. Our findings revealed that myh6 defects in zebrafish led to impaired atrial and ventricular function and disordered sarcomere. This research underscores the pivotal role of MYH6 in maintaining atrial function and development. The observed connections between sarcomeric gene variants and atrial cardiomyopathy contribute to our understanding of the genetic basis of atrial fibrillation.", null, null, null, "WT 2", "Sample 2", null, "strain:not collected|isolate:not collected|breed:not collected|cultivar:not collected|ecotype:not collected|age:6 mpf|dev stage:not collected|collection date:2023 09 03|geo loc name:not collected|sex:pooled male and female|tissue:heart|genotype:wild type|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "WT 2", "Sample 2", "Sample 2", "Sequencing data were analyzed by R studio Version 2023.03.0+386. 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MYH6 encodes a myosin heavy chain a MHC  predominantly expressed in the atria and pivotal in sarcomere organization and muscle contraction. However  the role of MYH6 in atrial diseases has not been fully elucidated and the genetic cause of atrial cardiomyopathy needs further investigation. Here  we employed CRISPR/Cas9 to generate myh6 knockout zebrafish  assessing cardiac function through diverse methodologies  including video analysis  ECG  echocardiography  transmission electron microscopy  and transcriptomic sequencing. Our findings revealed that myh6 defects in zebrafish led to impaired atrial and ventricular function and disordered sarcomere. This research underscores the pivotal role of MYH6 in maintaining atrial function and development. The observed connections between sarcomeric gene variants and atrial cardiomyopathy contribute to our understanding of the genetic basis of atrial fibrillation.", null, null, null, "WT 1", "Sample 1", null, "strain:not collected|isolate:not collected|breed:not collected|cultivar:not collected|ecotype:not collected|age:6 mpf|dev stage:not collected|collection date:2023 09 03|geo loc name:not collected|sex:pooled male and female|tissue:heart|genotype:wild type|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "WT 1", "Sample 1", "Sample 1", "Sequencing data were analyzed by R studio Version 2023.03.0+386. 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This project contains raw sequencing data sets that were used to identify that klf1  a Kruppel like transcription factor essential for red blood cell development  is also necessary and sufficient in the myocardium for the induction of cardiomyocyte dedifferentiation and proliferation in adult zebrafish hearts", null, null, "klf1 over expressing", null, "klf1", null, "strain:EKW|breed:n1|cultivar:n1|ecotype:n1|dev stage:Adult|sex:pooled male and female|tissue:hearts|genotype:klf1 overexpressing|sample type:tissue sample|treatment:untreated|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA Seq of zebrafish cardiac tissue", "OE4 RNASEQ", "OE4 RNASEQ", "Tissue was resuspended in 700ul Trizol and total RNA was extracted using miRNeasy kit following manufacturers description. Total RNA integrity was assessed and quantified on a RNA nano Agilent chip following manufacturers description. RNA libraries were prepared 500ng input using the Kapa stranded RNA Seq kit using the oligo dT module to enrich for mRNA transcripts. Libraries were pooled to equimolar concentrations and sequenced on an Illumina HiSeq2500 paired end reads using v4 high output chemistry.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina HiSeq 2500", null, "SRP211964", null, null, "CCB6CANXX_5_180204_CFL--007_Other_GATCAG_R_180116_DAVHUM_LIB2500_M003_R1.fastq.gz CCB6CANXX_5_180204_CFL--007_Other_GATCAG_R_180116_DAVHUM_LIB2500_M003_R2.fastq.gz", "fastq fastq", 7295330500.0, 29181322.0, "CCB6CANXX 5 180204 CFL  007 Other GATCAG R 180116 DAVHUM LIB2500 M003 R1.fastq.gz", "0:125 1:125", "A:2032530437;C:1615271949;G:1627524722;T:2018148293;N:1855099", 125, 125, null, null, 2032530437, 1615271949, 1627524722, 2018148293, 1855099, "SRX6362166", "SRS5024083", "SRA913571", "Victor Chang Cardiac Research Institute|Genome core", "Victor Chang Cardiac Research Institute", 2, 0.9317, 0.93743, 0.11776, 0.11755, 0.73497, 0.73888, 0.51221, 0.53503, 125, 125, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2019-06-26", "Adult", "Adult", "Heart", "Cardiovascular System"], [52920, "SRR9596464", "SRX6362165", "SRS5024084", "SRP211964", "PRJNA551130", "Induction of adult cardiomyocyte renewal by Klf1", "PRJNA551130", "Other", "In highly regenerative animals  cardiac regeneration occurs innately through cardiomyocyte dedifferentiation and proliferation  although the regenerative mechanisms remain unclear. This project contains raw sequencing data sets that were used to identify that klf1  a Kruppel like transcription factor essential for red blood cell development  is also necessary and sufficient in the myocardium for the induction of cardiomyocyte dedifferentiation and proliferation in adult zebrafish hearts", null, null, "WT", null, "WT", null, "strain:EKW|breed:n1|cultivar:n1|ecotype:n1|dev stage:Adult|sex:pooled male and female|tissue:hearts|genotype:WT|sample type:tissue sample|treatment:untreated|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA Seq of zebrafish cardiac tissue", "WT1 RNASEQ", "WT1 RNASEQ", "Tissue was resuspended in 700ul Trizol and total RNA was extracted using miRNeasy kit following manufacturers description. Total RNA integrity was assessed and quantified on a RNA nano Agilent chip following manufacturers description. RNA libraries were prepared 500ng input using the Kapa stranded RNA Seq kit using the oligo dT module to enrich for mRNA transcripts. Libraries were pooled to equimolar concentrations and sequenced on an Illumina HiSeq2500 paired end reads using v4 high output chemistry.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina HiSeq 2500", null, "SRP211964", null, null, "CCB6CANXX_5_180204_CFL--008_Other_TAGCTT_R_180116_DAVHUM_LIB2500_M003_R1.fastq.gz CCB6CANXX_5_180204_CFL--008_Other_TAGCTT_R_180116_DAVHUM_LIB2500_M003_R2.fastq.gz", "fastq fastq", 7309496000.0, 29237984.0, "CCB6CANXX 5 180204 CFL  008 Other TAGCTT R 180116 DAVHUM LIB2500 M003 R1.fastq.gz", "0:125 1:125", "A:2038562638;C:1607745758;G:1627387822;T:2033916634;N:1883148", 125, 125, null, null, 2038562638, 1607745758, 1627387822, 2033916634, 1883148, "SRX6362165", "SRS5024084", "SRA913571", "Victor Chang Cardiac Research Institute|Genome core", "Victor Chang Cardiac Research Institute", 2, 0.94874, 0.95324, 0.08149, 0.08128, 0.79356, 0.79575, 0.58607, 0.5765, 125, 125, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2019-06-26", "Adult", "Adult", "Heart", "Cardiovascular System"], [52921, "SRR9596465", "SRX6362164", "SRS5024084", "SRP211964", "PRJNA551130", "Induction of adult cardiomyocyte renewal by Klf1", "PRJNA551130", "Other", "In highly regenerative animals  cardiac regeneration occurs innately through cardiomyocyte dedifferentiation and proliferation  although the regenerative mechanisms remain unclear. This project contains raw sequencing data sets that were used to identify that klf1  a Kruppel like transcription factor essential for red blood cell development  is also necessary and sufficient in the myocardium for the induction of cardiomyocyte dedifferentiation and proliferation in adult zebrafish hearts", null, null, "WT", null, "WT", null, "strain:EKW|breed:n1|cultivar:n1|ecotype:n1|dev stage:Adult|sex:pooled male and female|tissue:hearts|genotype:WT|sample type:tissue sample|treatment:untreated|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA Seq of zebrafish cardiac tissue", "WT2 RNASEQ", "WT2 RNASEQ", "Tissue was resuspended in 700ul Trizol and total RNA was extracted using miRNeasy kit following manufacturers description. Total RNA integrity was assessed and quantified on a RNA nano Agilent chip following manufacturers description. RNA libraries were prepared 500ng input using the Kapa stranded RNA Seq kit using the oligo dT module to enrich for mRNA transcripts. Libraries were pooled to equimolar concentrations and sequenced on an Illumina HiSeq2500 paired end reads using v4 high output chemistry.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina HiSeq 2500", null, "SRP211964", null, null, "CCB6CANXX_5_180204_CFL--009_Other_GGCTAC_R_180116_DAVHUM_LIB2500_M003_R1.fastq.gz CCB6CANXX_5_180204_CFL--009_Other_GGCTAC_R_180116_DAVHUM_LIB2500_M003_R2.fastq.gz", "fastq fastq", 6324176500.0, 25296706.0, "CCB6CANXX 5 180204 CFL  009 Other GGCTAC R 180116 DAVHUM LIB2500 M003 R1.fastq.gz", "0:125 1:125", "A:1766296515;C:1389598935;G:1403023173;T:1763639041;N:1618836", 125, 125, null, null, 1766296515, 1389598935, 1403023173, 1763639041, 1618836, "SRX6362164", "SRS5024084", "SRA913571", "Victor Chang Cardiac Research Institute|Genome core", "Victor Chang Cardiac Research Institute", 2, 0.94374, 0.94892, 0.09048, 0.09084, 0.78681, 0.79066, 0.57761, 0.5755, 125, 125, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2019-06-26", "Adult", "Adult", "Heart", "Cardiovascular System"], [52922, "SRR9596466", "SRX6362163", "SRS5024084", "SRP211964", "PRJNA551130", "Induction of adult cardiomyocyte renewal by Klf1", "PRJNA551130", "Other", "In highly regenerative animals  cardiac regeneration occurs innately through cardiomyocyte dedifferentiation and proliferation  although the regenerative mechanisms remain unclear. This project contains raw sequencing data sets that were used to identify that klf1  a Kruppel like transcription factor essential for red blood cell development  is also necessary and sufficient in the myocardium for the induction of cardiomyocyte dedifferentiation and proliferation in adult zebrafish hearts", null, null, "WT", null, "WT", null, "strain:EKW|breed:n1|cultivar:n1|ecotype:n1|dev stage:Adult|sex:pooled male and female|tissue:hearts|genotype:WT|sample type:tissue sample|treatment:untreated|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA Seq of zebrafish cardiac tissue", "WT3 RNASEQ", "WT3 RNASEQ", "Tissue was resuspended in 700ul Trizol and total RNA was extracted using miRNeasy kit following manufacturers description. Total RNA integrity was assessed and quantified on a RNA nano Agilent chip following manufacturers description. RNA libraries were prepared 500ng input using the Kapa stranded RNA Seq kit using the oligo dT module to enrich for mRNA transcripts. Libraries were pooled to equimolar concentrations and sequenced on an Illumina HiSeq2500 paired end reads using v4 high output chemistry.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina HiSeq 2500", null, "SRP211964", null, null, "CCB6CANXX_5_180204_CFL--010_Other_GTGGCC_R_180116_DAVHUM_LIB2500_M003_R1.fastq.gz CCB6CANXX_5_180204_CFL--010_Other_GTGGCC_R_180116_DAVHUM_LIB2500_M003_R2.fastq.gz", "fastq fastq", 7057191250.0, 28228765.0, "CCB6CANXX 5 180204 CFL  010 Other GTGGCC R 180116 DAVHUM LIB2500 M003 R1.fastq.gz", "0:125 1:125", "A:1983309478;C:1539045596;G:1559191474;T:1973857420;N:1787282", 125, 125, null, null, 1983309478, 1539045596, 1559191474, 1973857420, 1787282, "SRX6362163", "SRS5024084", "SRA913571", "Victor Chang Cardiac Research Institute|Genome core", "Victor Chang Cardiac Research Institute", 2, 0.94841, 0.95328, 0.08661, 0.08555, 0.78936, 0.79243, 0.58731, 0.61025, 125, 125, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2019-06-26", "Adult", "Adult", "Heart", "Cardiovascular System"], [52923, "SRR9596467", "SRX6362162", "SRS5024084", "SRP211964", "PRJNA551130", "Induction of adult cardiomyocyte renewal by Klf1", "PRJNA551130", "Other", "In highly regenerative animals  cardiac regeneration occurs innately through cardiomyocyte dedifferentiation and proliferation  although the regenerative mechanisms remain unclear. This project contains raw sequencing data sets that were used to identify that klf1  a Kruppel like transcription factor essential for red blood cell development  is also necessary and sufficient in the myocardium for the induction of cardiomyocyte dedifferentiation and proliferation in adult zebrafish hearts", null, null, "WT", null, "WT", null, "strain:EKW|breed:n1|cultivar:n1|ecotype:n1|dev stage:Adult|sex:pooled male and female|tissue:hearts|genotype:WT|sample type:tissue sample|treatment:untreated|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA Seq of zebrafish cardiac tissue", "WT4 RNASEQ", "WT4 RNASEQ", "Tissue was resuspended in 700ul Trizol and total RNA was extracted using miRNeasy kit following manufacturers description. Total RNA integrity was assessed and quantified on a RNA nano Agilent chip following manufacturers description. RNA libraries were prepared 500ng input using the Kapa stranded RNA Seq kit using the oligo dT module to enrich for mRNA transcripts. Libraries were pooled to equimolar concentrations and sequenced on an Illumina HiSeq2500 paired end reads using v4 high output chemistry.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina HiSeq 2500", null, "SRP211964", null, null, "CCB6CANXX_5_180204_CFL--011_Other_GTTTCG_R_180116_DAVHUM_LIB2500_M003_R1.fastq.gz CCB6CANXX_5_180204_CFL--011_Other_GTTTCG_R_180116_DAVHUM_LIB2500_M003_R2.fastq.gz", "fastq fastq", 6296219250.0, 25184877.0, "CCB6CANXX 5 180204 CFL  011 Other GTTTCG R 180116 DAVHUM LIB2500 M003 R1.fastq.gz", "0:125 1:125", "A:1758686297;C:1380462937;G:1398800047;T:1756652381;N:1617588", 125, 125, null, null, 1758686297, 1380462937, 1398800047, 1756652381, 1617588, "SRX6362162", "SRS5024084", "SRA913571", "Victor Chang Cardiac Research Institute|Genome core", "Victor Chang Cardiac Research Institute", 2, 0.94465, 0.94985, 0.09014, 0.08958, 0.78151, 0.78472, 0.58358, 0.58306, 125, 125, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2019-06-26", "Adult", "Adult", "Heart", "Cardiovascular System"], [68887, "SRR18218065", "SRX14364509", "SRS12177804", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "CG1 P2mut STABLE 5", null, "strain:CG1|age:133 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:23 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 5|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1", "CG1 P2mut STABLE 5", "CG1 P2mut STABLE 5", "CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAAURAAPEI-P51E3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAURAAPEI-P51E3_2.fq.gz", "fastq fastq", 18195264000.0, 60650880.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAAURAAPEI P51E3 1.fq.gz", "0:150 1:150", "A:4675448937;C:4456563746;G:4459950645;T:4603273696;N:26976", 150, 150, null, null, 4675448937, 4456563746, 4459950645, 4603273696, 26976, "SRX14364509", "SRS12177804", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.94521, 0.94594, 0.11243, 0.11174, 0.79551, 0.79496, 0.51393, 0.51099, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Adult", "Adult", "Lymphatic System", "Cardiovascular System"], [68888, "SRR18218066", "SRX14364508", "SRS12177803", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "CG1 P2mut STABLE 4", null, "strain:CG1|age:133 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:23 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 4|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1", "CG1 P2mut STABLE 4", "CG1 P2mut STABLE 4", "CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAATRAAPEI-P39D3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAATRAAPEI-P39D3_2.fq.gz", "fastq fastq", 18145191600.0, 60483972.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAATRAAPEI P39D3 1.fq.gz", "0:150 1:150", "A:4669829222;C:4433244502;G:4437119015;T:4604972909;N:25952", 150, 150, null, null, 4669829222, 4433244502, 4437119015, 4604972909, 25952, "SRX14364508", "SRS12177803", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.94405, 0.94389, 0.11135, 0.11157, 0.79401, 0.79385, 0.50436, 0.50132, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Adult", "Adult", "Lymphatic System", "Cardiovascular System"], [68893, "SRR18218072", "SRX14364503", "SRS12177798", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "Tu AB mMyc 7", null, "strain:Tu/AB|age:41 days|sex:not collected|tissue:lymphoid|birth date:04 11 2016|death date:15 12 2016|genotype:rag2:mCherry rag2:mMyc|biological replicate:Tu AB mMyc biological replicate 3|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia overexpressing mouse Myc Tu/AB", "Tu AB mMyc 7", "Tu AB mMyc 7", "Tu/AB zebrafish overexpressing mouse Myc transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAAXRAAPEI-P87H3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAXRAAPEI-P87H3_2.fq.gz", "fastq fastq", 18002105400.0, 60007018.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAAXRAAPEI P87H3 1.fq.gz", "0:150 1:150", "A:4483057959;C:4549819065;G:4562924506;T:4406277865;N:26005", 150, 150, null, null, 4483057959, 4549819065, 4562924506, 4406277865, 26005, "SRX14364503", "SRS12177798", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.9259, 0.92681, 0.09642, 0.09697, 0.82479, 0.82546, 0.50634, 0.5148, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Juvenile", "Juvenile", "Lymphatic System", "Cardiovascular System"], [68894, "SRR18218073", "SRX14364502", "SRS12177797", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "Tu AB mMyc 6", null, "strain:Tu/AB|age:42 days|sex:not collected|tissue:lymphoid|birth date:03 11 2016|death date:15 12 2016|genotype:rag2:mCherry rag2:mMyc|biological replicate:Tu AB mMyc biological replicate 2|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia overexpressing mouse Myc Tu/AB", "Tu AB mMyc 6", "Tu AB mMyc 6", "Tu/AB zebrafish overexpressing mouse Myc transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAAWRABPEI-P75G3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAWRABPEI-P75G3_2.fq.gz", "fastq fastq", 18085463400.0, 60284878.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAAWRABPEI P75G3 1.fq.gz", "0:150 1:150", "A:4716166539;C:4371919988;G:4399782048;T:4597568953;N:25872", 150, 150, null, null, 4716166539, 4371919988, 4399782048, 4597568953, 25872, "SRX14364502", "SRS12177797", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.90432, 0.90596, 0.06444, 0.06367, 0.80048, 0.80095, 0.51671, 0.51624, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Juvenile", "Juvenile", "Lymphatic System", "Cardiovascular System"], [68895, "SRR18218074", "SRX14364501", "SRS12177796", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "Tu AB mMyc 5", null, "strain:Tu/AB|age:42 days|sex:not collected|tissue:lymphoid|birth date:03 11 2016|death date:15 12 2016|genotype:rag2:mCherry rag2:mMyc|biological replicate:Tu AB mMyc biological replicate 1|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia overexpressing mouse Myc Tu/AB", "Tu AB mMyc 5", "Tu AB mMyc 5", "Tu/AB zebrafish overexpressing mouse Myc transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAAVRAAPEI-P63F3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAVRAAPEI-P63F3_2.fq.gz", "fastq fastq", 18063312600.0, 60211042.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAAVRAAPEI P63F3 1.fq.gz", "0:150 1:150", "A:4440821008;C:4618318980;G:4635597240;T:4368548938;N:26434", 150, 150, null, null, 4440821008, 4618318980, 4635597240, 4368548938, 26434, "SRX14364501", "SRS12177796", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.91708, 0.91735, 0.0319, 0.0316, 0.80793, 0.80744, 0.50004, 0.5071, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Juvenile", "Juvenile", "Lymphatic System", "Cardiovascular System"], [68896, "SRR18218075", "SRX14364500", "SRS12177795", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "CG1 P2mut STABLE 3", null, "strain:CG1|age:121 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:11 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 3|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1", "CG1 P2mut STABLE 3", "CG1 P2mut STABLE 3", "CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAASRAAPEI-P27C3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAASRAAPEI-P27C3_2.fq.gz", "fastq fastq", 18163928100.0, 60546427.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAASRAAPEI P27C3 1.fq.gz", "0:150 1:150", "A:4642188606;C:4470457895;G:4476885626;T:4574370149;N:25824", 150, 150, null, null, 4642188606, 4470457895, 4476885626, 4574370149, 25824, "SRX14364500", "SRS12177795", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.94449, 0.94468, 0.0858, 0.0861, 0.77114, 0.7696, 0.52498, 0.52464, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Adult", "Adult", "Lymphatic System", "Cardiovascular System"], [68897, "SRR18218076", "SRX14364499", "SRS12177794", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "Tu AB mMyc+P2mut 4", null, "strain:Tu/AB|age:28 days|sex:not collected|tissue:lymphoid|birth date:08 02 2017|death date:08 03 2017|genotype:rag2:mCherry rag2:mMyc rag2:hIL7R mut2|biological replicate:Tu AB mMyc+P1mut biological replicate 4|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia overexpressing mouse Myc and human mutant IL7R Tu/AB", "Tu AB mMyc+P2mut 4", "Tu AB mMyc+P2mut 4", "Tu/AB zebrafish overexpressing mouse Myc and human mutant IL7R transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEABBRAAPEI-P40D4_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEABBRAAPEI-P40D4_2.fq.gz", "fastq fastq", 18117791400.0, 60392638.0, "FCHT5GHDSXX L1 HKRDZEBmfpEABBRAAPEI P40D4 1.fq.gz", "0:150 1:150", "A:4565894721;C:4513701269;G:4551999162;T:4486169550;N:26698", 150, 150, null, null, 4565894721, 4513701269, 4551999162, 4486169550, 26698, "SRX14364499", "SRS12177794", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.94, 0.93956, 0.08699, 0.08679, 0.81941, 0.81832, 0.51722, 0.51946, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Larval", "Larval", "Lymphatic System", "Cardiovascular System"], [68898, "SRR18218077", "SRX14364498", "SRS12177793", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "Tu AB mMyc+P1mut 6", null, "strain:Tu/AB|age:35 days|sex:not collected|tissue:lymphoid|birth date:30 08 2016|death date:04 10 2016|genotype:rag2:mCherry rag2:mMyc rag2:hIL7R mut1|biological replicate:Tu AB mMyc+P1mut biological replicate 3|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia overexpressing mouse Myc and human mutant IL7R Tu/AB", "Tu AB mMyc+P1mut 6", "Tu AB mMyc+P1mut 6", "Tu/AB zebrafish overexpressing mouse Myc and human mutant IL7R transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEABARAAPEI-P28C4_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEABARAAPEI-P28C4_2.fq.gz", "fastq fastq", 18034321800.0, 60114406.0, "FCHT5GHDSXX L1 HKRDZEBmfpEABARAAPEI P28C4 1.fq.gz", "0:150 1:150", "A:4518122158;C:4519676234;G:4543758117;T:4452738564;N:26727", 150, 150, null, null, 4518122158, 4519676234, 4543758117, 4452738564, 26727, "SRX14364498", "SRS12177793", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.94431, 0.94437, 0.10494, 0.10462, 0.83177, 0.83037, 0.51143, 0.51642, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Juvenile", "Juvenile", "Lymphatic System", "Cardiovascular System"], [68899, "SRR18218078", "SRX14364497", "SRS12177792", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "Tu AB mMyc+P1mut 5", null, "strain:Tu/AB|age:35 days|sex:not collected|tissue:lymphoid|birth date:30 08 2016|death date:04 10 2016|genotype:rag2:mCherry rag2:mMyc rag2:hIL7R mut1|biological replicate:Tu AB mMyc+P1mut biological replicate 2|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia overexpressing mouse Myc and human mutant IL7R Tu/AB", "Tu AB mMyc+P1mut 5", "Tu AB mMyc+P1mut 5", "Tu/AB zebrafish overexpressing mouse Myc and human mutant IL7R transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAAZRAAPEI-P16B4_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAZRAAPEI-P16B4_2.fq.gz", "fastq fastq", 17750634300.0, 59168781.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAAZRAAPEI P16B4 1.fq.gz", "0:150 1:150", "A:4503506819;C:4398697723;G:4432972998;T:4415430837;N:25923", 150, 150, null, null, 4503506819, 4398697723, 4432972998, 4415430837, 25923, "SRX14364497", "SRS12177792", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.94306, 0.94321, 0.07511, 0.0748, 0.79837, 0.79819, 0.51326, 0.50902, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Juvenile", "Juvenile", "Lymphatic System", "Cardiovascular System"], [68900, "SRR18218079", "SRX14364496", "SRS12177791", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "Tu AB mMyc+P1mut 4", null, "strain:Tu/AB|age:35 days|sex:not collected|tissue:lymphoid|birth date:30 08 2016|death date:04 10 2016|genotype:rag2:mCherry rag2:mMyc rag2:hIL7R mut1|biological replicate:Tu AB mMyc+P1mut biological replicate 1|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia overexpressing mouse Myc and human mutant IL7R Tu/AB", "Tu AB mMyc+P1mut 4", "Tu AB mMyc+P1mut 4", "Tu/AB zebrafish overexpressing mouse Myc and human mutant IL7R transiently were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAAYRAAPEI-P4A4_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAYRAAPEI-P4A4_2.fq.gz", "fastq fastq", 18063110700.0, 60210369.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAAYRAAPEI P4A4 1.fq.gz", "0:150 1:150", "A:4583950532;C:4496933352;G:4489104841;T:4493095718;N:26257", 150, 150, null, null, 4583950532, 4496933352, 4489104841, 4493095718, 26257, "SRX14364496", "SRS12177791", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.95231, 0.9534, 0.12525, 0.12554, 0.84404, 0.84323, 0.52132, 0.53078, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Juvenile", "Juvenile", "Lymphatic System", "Cardiovascular System"], [68911, "SRR18218090", "SRX14364485", "SRS12177780", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "CG1 P2mut STABLE 2", null, "strain:CG1|age:121 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:11 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 2|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1", "CG1 P2mut STABLE 2", "CG1 P2mut STABLE 2", "CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAARRAAPEI-P15B3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAARRAAPEI-P15B3_2.fq.gz", "fastq fastq", 18103313700.0, 60344379.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAARRAAPEI P15B3 1.fq.gz", "0:150 1:150", "A:4586370941;C:4481640272;G:4519408464;T:4515867439;N:26584", 150, 150, null, null, 4586370941, 4481640272, 4519408464, 4515867439, 26584, "SRX14364485", "SRS12177780", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.94376, 0.94365, 0.11084, 0.10978, 0.79847, 0.79788, 0.52621, 0.52367, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Adult", "Adult", "Lymphatic System", "Cardiovascular System"], [68912, "SRR18218091", "SRX14364484", "SRS12177779", "SRP362416", "PRJNA812715", "Mutant IL7R collaborates with MYC to induce  T cell Acute Lymphoblastic Leukemia", "PRJNA812715", "Other", "T cell acute lymphoblastic leukemia T ALL is an aggressive pediatric cancer. Amongst the wide array of driver mutations  10% of T ALL patients display gain of function mutations in the IL 7 receptor alpha chain IL 7Ralpha  encoded by IL7R  which occur in different molecular subtypes of this disease. However  it is still unclear whether IL 7R mutational activation is sufficient to transform T cell precursors. Also  which genes cooperate with IL7R to drive leukemogenesis remain poorly defined. Here  we demonstrate that mutant IL7R alone is capable of inducing T ALL with long latency in stable transgenic zebrafish and transformation is associated with MYC transcriptional activation. Additionally  we find that mutant IL7R collaborates with Myc to induce early onset T ALL in transgenic zebrafish. T ALLs co expressing mutant IL7R and Myc show activation of STAT5 and AKT pathways  harbor reduced numbers of apoptotic cells and remake tumors in transplanted zebrafish faster than T ALLs expressing Myc alone. Moreover  limiting dilution cell transplantation experiments reveal that activated IL 7R signaling increases the overall frequency of leukemia propagating cells. Our work highlights a synergy between mutant IL7R and Myc in inducing T ALL and demonstrates that mutant IL7R enriches for leukemia propagating potential.", null, null, null, null, "CG1 P2mut STABLE 1", null, "strain:CG1|age:121 days|sex:not collected|tissue:lymphoid|birth date:12 04 2017|death date:11 08 2017|genotype:rag2:hIL7R mut2 tdTomato|biological replicate:CG1 P2mut STABLE biologicalreplicate 1|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq of Danio rerio leukemia stably expressing human mutant IL7R CG1", "CG1 P2mut STABLE 1", "CG1 P2mut STABLE 1", "CG1 zebrafish stably expressing human mutant IL7R were sacrificed when moribund and sorted leukemias were harvested for further analysis. The RNA was extracted from sorted cells using the RNeasy Mini Kit according to the manufacturers instructions Qiagen. mRNA was enriched using magnetic beads with Oligo dT  fragmented and converted to cDNA  size selected and PCR amplified generating paired end 100 bp sequences using a Illumina NovaSeq 6000.", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "PolyA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP362416", null, null, "FCHT5GHDSXX_L1_HKRDZEBmfpEAAQRAAPEI-P3A3_1.fq.gz FCHT5GHDSXX_L1_HKRDZEBmfpEAAQRAAPEI-P3A3_2.fq.gz", "fastq fastq", 18068692800.0, 60228976.0, "FCHT5GHDSXX L1 HKRDZEBmfpEAAQRAAPEI P3A3 1.fq.gz", "0:150 1:150", "A:4592071905;C:4477973011;G:4471601663;T:4527019823;N:26398", 150, 150, null, null, 4592071905, 4477973011, 4471601663, 4527019823, 26398, "SRX14364484", "SRS12177779", "SRA1380603", "Instituto de Medicina Molecular Joao Lobo Antunes|JBarata lab", "Instituto de Medicina Molecular Joao Lobo Antunes", 2, 0.94814, 0.94931, 0.09511, 0.09463, 0.79756, 0.79762, 0.51602, 0.51609, 150, 150, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "poly_a", "unknown", "bulk", "unknown", "unknown", null, "Portugal", "2022-03-04", "Adult", "Adult", "Lymphatic System", "Cardiovascular System"]], "truncated": false, "filtered_table_rows_count": 26, "expanded_columns": [], "expandable_columns": [], "columns": ["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"], "primary_keys": [], "units": {}, "query": {"sql": "select 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 from run_metadata where \"experiment.library_selection\" = :p0 and \"technology\" = :p1 and \"tissue_curation_coarse\" = :p2 order by rowid limit 101", "params": {"p0": "PolyA", "p1": "unknown", "p2": "Cardiovascular System"}}, "facet_results": {"experiment.library_strategy": {"name": "experiment.library_strategy", "type": "column", "hideable": false, "toggle_url": "/metadata/run_metadata.json?experiment.library_selection=PolyA&technology=unknown&tissue_curation_coarse=Cardiovascular+System", "results": [{"value": "RNA-Seq", "label": "RNA-Seq", "count": 26, "toggle_url": "http://metadata.rnaquarium.org/metadata/run_metadata.json?experiment.library_selection=PolyA&technology=unknown&tissue_curation_coarse=Cardiovascular+System&experiment.library_strategy=RNA-Seq", "selected": false}], "truncated": false}, "experiment.library_source": {"name": "experiment.library_source", "type": "column", "hideable": false, "toggle_url": "/metadata/run_metadata.json?experiment.library_selection=PolyA&technology=unknown&tissue_curation_coarse=Cardiovascular+System", "results": [{"value": "TRANSCRIPTOMIC", "label": "TRANSCRIPTOMIC", "count": 26, "toggle_url": "http://metadata.rnaquarium.org/metadata/run_metadata.json?experiment.library_selection=PolyA&technology=unknown&tissue_curation_coarse=Cardiovascular+System&experiment.library_source=TRANSCRIPTOMIC", 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