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Publication : JMJD1C is required for the survival of acute myeloid leukemia by functioning as a coactivator for key transcription factors.

First Author  Chen M Year  2015
Journal  Genes Dev Volume  29
Issue  20 Pages  2123-39
PubMed ID  26494788 Mgi Jnum  J:226613
Mgi Id  MGI:5697985 Doi  10.1101/gad.267278.115
Citation  Chen M, et al. (2015) JMJD1C is required for the survival of acute myeloid leukemia by functioning as a coactivator for key transcription factors. Genes Dev 29(20):2123-39
abstractText  RUNX1-RUNX1T1 (formerly AML1-ETO), a transcription factor generated by the t(8;21) translocation in acute myeloid leukemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a coactivator for RUNX1-RUNX1T1 and is required for its transcriptional program. JMJD1C is directly recruited by RUNX1-RUNX1T1 to its target genes and regulates their expression by maintaining low H3K9 dimethyl (H3K9me2) levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for RUNX1-RUNX1T1'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.
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