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Aberrant chromatin acetylation in MLL-AF9 leukemia mediates the response to HDAC inhibition (microarray). Homo sapiens

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https://www.ncbi.nlm.nih.gov/bioproject/PRJNA236219
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We investigated the response of acute myeloid cells (AML) expressing MLL-AF9 fusion gene to the pan-HDACi panobinostat (LBH589), and found that low conentrations of panobinostat lead to MLL-AF9 cell toxicity and rapid changes in gene expression. Human hematopoietic stem/progenitor cells (HSPC) expressing MLL-AF9 fusion protein (Wei et al, Cancer Cell 2008) were cultured with 30 nM panobinostat during 6 and 24 hours. The different gene expression between cells treated and untreated was studied by gene expression analysis. Overall design: Three independent HSPC-MA9 clones were used, for each two replicates of cells after culture with 30 nM panobinostat for 6 and 24 hours and one untreated were used. A total of 16 samples were analyzed.
创建时间:
2014-01-20
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