Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA215939 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:shRNA Screening Identifies JMJD1C as being required for Leukemia Maintenance (Agilent)
| PRJNA236136 | ENA
Project description:The roles of histone demethylases (HDMs) for the establishment and maintenance of the pluripotent state are incompletely defined. Here, we show that JmjC domain-containing protein 1c (Jmjd1c), a putative histone H3 Lys 9 (H3K9) demethylase, is required for mouse embryonic stem cell (ESC) self-renewal. To understand how Jmjd1c knockdown (KD) and resultant changes in the H3K9 methylations would affect ESCs at a global gene expression level, we compared the whole genome transcriptomes between the control and Jmjd1c KD ESCs (6 samples, including 2 shNT control samples and 4 shJmjd1c samples, 2 from #3 and 2 from #4 shRNA, respectively) using affymetrix microarray. We used microarrays to identify genes affected by Jmjd1c knockdown in mouse ESCs.
2017-07-24 | GSE89709 | GEO
Project description:We used a mouse model of human AML induced by the MLL-AF9 fusion oncogene, and an epigenetic shRNA library to screen for novel potential drug targets. One of the best candidate drug targets identified in these screens was Jmjd1c. Depletion of Jmjd1c impairs growth and colony formation of mouse MLL-AF9 cells in vitro, as well as establishment of leukemia after transplantation. Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line, SEM. In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primarily due to increased apoptosis, which implicates JMJD1C as a potential therapeutic target in leukemia. To assess the effect of JMJD1C depletion on transcription, we compared the transcriptome of shJMJD1C- and shScr-transduced SEM cells soon after induction of shRNA expression by addition of IPTG to the growth medium. To ensure detecting early changes, 48h was selected as the earliest timepoint displaying JMJD1C depletion and detectable phenotype as monitored by PARP and Caspase 3 cleavage. These observations were consistent across triplicate samples. A total of 138 transcripts were detected as changing between the two conditions (FDR<0.05)
2013-08-22 | E-GEOD-50048 | biostudies-arrayexpress
Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETOâs ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors. Examination of RNA expression when Kasumi-1 cells are treated with control shRNA or two different JMJD1C shRNAs; in duplicate. Please note that the 'shAML1_ETO_vs_shControl.all_gene_exp.tb.txtl' was generated comparing control and shRNA treated RNA abundance-using previously published data [GSE43834; GSM1071857 and GSM1071852].
2015-11-02 | E-GEOD-63485 | biostudies-arrayexpress
Project description:We used a mouse model of human AML induced by the MLL-AF9 fusion oncogene, and an epigenetic shRNA library to screen for novel potential drug targets. One of the best candidate drug targets identified in these screens was Jmjd1c. Depletion of Jmjd1c impairs growth and colony formation of mouse MLL-AF9 cells in vitro, as well as establishment of leukemia after transplantation. Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line, SEM. In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primarily due to increased apoptosis, which implicates JMJD1C as a potential therapeutic target in leukemia. To assess the effect of JMJD1C depletion on transcription, we compared the transcriptome of shJMJD1C- and shScr-transduced mouse MLL-AF9 transformed cells 48h after infection. A total of 451 transcripts were detected as changing between the two conditions (FDR<0.25)
2014-01-23 | E-GEOD-54311 | biostudies-arrayexpress
Project description:We used a mouse model of human AML induced by the MLL-AF9 fusion oncogene, and an epigenetic shRNA library to screen for novel potential drug targets. One of the best candidate drug targets identified in these screens was Jmjd1c. Depletion of Jmjd1c impairs growth and colony formation of mouse MLL-AF9 cells in vitro, as well as establishment of leukemia after transplantation. Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line, SEM. In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primarily due to increased apoptosis, which implicates JMJD1C as a potential therapeutic target in leukemia.
2013-08-22 | GSE50048 | GEO
Project description:We used a mouse model of human AML induced by the MLL-AF9 fusion oncogene, and an epigenetic shRNA library to screen for novel potential drug targets. One of the best candidate drug targets identified in these screens was Jmjd1c. Depletion of Jmjd1c impairs growth and colony formation of mouse MLL-AF9 cells in vitro, as well as establishment of leukemia after transplantation. Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line, SEM. In both mouse and human leukemic cells, the growth defect upon JMJD1C depletion appears to be primarily due to increased apoptosis, which implicates JMJD1C as a potential therapeutic target in leukemia.
2014-01-23 | GSE54311 | GEO
Project description:The mechanisms whereby the crucial pluripotency transcription factor Oct4 regulates target gene expression are incompletely understood. Using an assay system based on partially differentiated embryonic stem cells, we show that Oct4 opposes accumulation of local H3K9me2, and subsequent Dnmt3a-mediated DNA methylation. Upon binding DNA, Oct4 recruits the histone lysine demethylase Jmjd1c. ChIP timecourse experiments identify a stepwise Oct4 mechanism involving Jmjd1c recruitment and H3K9me2 demethylation, transient FACT complex recruitment, and nucleosome depletion. Genome-wide and targeted ChIP confirms binding of newly-synthesized Oct4, together with Jmjd1c and FACT, to the Pou5f1 enhancer and a small number of other Oct4 targets, including the Nanog promoter. Histone demethylation is required for both FACT recruitment and H3 depletion. Jmjd1c is required to induce endogenous Oct4 expression and fully reprogram fibroblasts to pluripotency, indicating that the assay system identifies functional Oct4 cofactors. These findings indicate that Oct4 sequentially recruits activities that catalyze histone demethylation and depletion. Examination of transcription factor occupancy in cells with newly synthesized Oct4.
2015-01-23 | E-GEOD-65192 | biostudies-arrayexpress
Project description:shRNA screen identifies lncRNAs required for acute myeloid leukemia progresion
| PRJNA354550 | ENA
Project description:Analysis of gene expression profile of MLL-AF9 leukemia cells 6 days after loss of Jmjd1c. Loss of Jmjd1c induces differentiation and apoptosis in MLL-AF9 leukemia cells. These results provide insight into the role of Jmjd1c in MLL leukemia.
2016-06-09 | GSE75576 | GEO