HRP2-MINA complex reprograms t(4;14) multiple myeloma epigenome to dictate chemosensitivity to proteasome inhibitors [ChIP-Seq]
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https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE166526
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Changes in these genes are probably a consequence of aging, and the real regulators governing BMSC senescence and osteogenesis are still unclear.In the current study, we report that nucleosome assembly-related protein NAP1L2 serves as an important regulator of both the senescence and osteogenic differentiation of BMSCs through inhibition of NF-κB signaling and recruitment of SIRT1 to deacetylate the H3K14ac level on promoters of osteogenic genes. Thus, targeting NAP1L2 using an aging antagonist such as NMN would benefit aging-related disease. Examination of histone modification in non-target control and knockdown HRP2 LP-1 cells and HRP2 modification in LP-1 cells
创建时间：
2021-02-13
