Similar Datasets
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 JMJD1C and LYL1 chromatin binding in Kasumi-1 cells, HL-60 cells, NB-4 cells and THP-1 cells, including ChIP-seqs of JMJD1C and LYL1, and input DNAs for Kasumi-1, HL-60, NB4.
2015-11-02 | E-GEOD-63484 | 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: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-ETO’s 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.
2015-11-02 | GSE63485 | GEO
Project description:It has been recently reported that the pluripotency factor OCT4, the early neural inducing factor NR2F2, and the pluripotency-associated miRNA miR-302 are linked in a regulatory circuitry that critically regulate both pluripotency and neural differentiation of human embryonic stem cells (hESCs). We show here that JMJD1C, a H3K9 demethylase expressed in undifferentiated hESCs, plays a key role in the regulatory circuitry. hESCs with JMJD1C knockdown (KD) retain the state of self-renewal and pluripotency, but express lower miR-302c than control hESCs. JMJD1C directly binds to the miR-302 promoter in hESCs and reduces H3K9 methylation on the promoter. Upon withdrawal of bFGF (an inhibitor of neural initiation) from a defined culture medium, the KD, but not control, hESCs differentiate into neural progenitors within three days – the fastest ever reported, accompanied by rapid increase of NR2F2 expression. A miR-302c analogue or an inhibitor of H3K9 methylation reduces neural induction from the KD hESCs, whereas a miR-302c inhibitor promotes hESC differentiation. Together, our findings suggest that JMJD1C plays a central role in control of neural differentiation from hESCs, which involves sustained miR-302c expression, and that inhibition of JMJD1C is sufficient to rapidly induce neural progenitors from hESCs in the defined medium depleted of bFGF. This is also the first evidence, to our knowledge, for epigenetic modification of miR-302 in hESCs. 6 human ES cell lines were used in this microarray assay. Each line has two replicates.
2013-12-24 | E-GEOD-46485 | biostudies-arrayexpress
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
Project description:JMJD1C, a Jumonji C (JmjC) domain-containing histone demethylase, has been reported as a direct cofactor of oncogenic transcription factor HOXA9. To identify JMJD1C downstream effectors, we performed a genome-wide gene expression profiling experiment. Our microarray analysis identified a new role for JMJD1C in regulating a cancer metabolic program in HOX-driven AML. GFP+ HOXA9/MEIS1-mediated pre-leukemic stem cells were transduced with retroviruses carrying JMJD1C or empty vector for the microarray experiment. Each group has 4 samples.
2018-12-30 | E-MTAB-5760 | biostudies-arrayexpress
Project description:Analysis of gene expression profile of Hoxa9/Meis1 leukemia cells 6 days after loss of Jmjd1c. Loss of Jmjd1c induces differentiation and Hoxa9/Meis1 leukemia cells. These results provide insight into the role of Jmjd1c in AML with elelvated expression of Hoxa9.
2016-06-09 | GSE75580 | GEO
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-ETO’s 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.
2015-11-02 | GSE63484 | GEO
Project description:It has been recently reported that the pluripotency factor OCT4, the early neural inducing factor NR2F2, and the pluripotency-associated miRNA miR-302 are linked in a regulatory circuitry that critically regulate both pluripotency and neural differentiation of human embryonic stem cells (hESCs). We show here that JMJD1C, a H3K9 demethylase expressed in undifferentiated hESCs, plays a key role in the regulatory circuitry. hESCs with JMJD1C knockdown (KD) retain the state of self-renewal and pluripotency, but express lower miR-302c than control hESCs. JMJD1C directly binds to the miR-302 promoter in hESCs and reduces H3K9 methylation on the promoter. Upon withdrawal of bFGF (an inhibitor of neural initiation) from a defined culture medium, the KD, but not control, hESCs differentiate into neural progenitors within three days – the fastest ever reported, accompanied by rapid increase of NR2F2 expression. A miR-302c analogue or an inhibitor of H3K9 methylation reduces neural induction from the KD hESCs, whereas a miR-302c inhibitor promotes hESC differentiation. Together, our findings suggest that JMJD1C plays a central role in control of neural differentiation from hESCs, which involves sustained miR-302c expression, and that inhibition of JMJD1C is sufficient to rapidly induce neural progenitors from hESCs in the defined medium depleted of bFGF. This is also the first evidence, to our knowledge, for epigenetic modification of miR-302 in hESCs.
2013-12-24 | GSE46485 | GEO
Project description:Analysis of gene expression profile of LSK (Lin-Sca-1+ c-Kit+) isolated from Jmjd1c f/f Vav1Cre or Vav1Cre controls. Loss of Jmjd1c minimally affected HSC in homeostatsis while impiars HSC function in response to stree such as transplantation and 5-Fu treatment. These results provide insight into the role of Jmjd1c in normal hematopoiesis.
2016-06-09 | GSE75579 | GEO