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- W2959431180 abstract "Abstract Acute myeloid leukemia (AML) is a genetically heterogeneous malignant disorder of the hematopoietic system, characterized by the accumulation of DNA-damaged immature myeloid precursors. Here, we find that hCINAP is involved in the repair of double-stranded DNA breaks (DSB) and that its expression correlates with AML prognosis. Following DSB, hCINAP is recruited to damage sites where it promotes SENP3-dependent deSUMOylation of NPM1. This in turn results in the dissociation of RAP80 from the damage site and CTIP-dependent DNA resection and homologous recombination. NPM1 SUMOylation is required for recruitment of DNA repair proteins at the early stage of DNA-damage response (DDR), and SUMOylated NPM1 impacts the assembly of the BRCA1 complex. Knockdown of hCINAP also sensitizes a patient-derived xenograft (PDX) mouse model to chemotherapy. In clinical AML samples, low hCINAP expression is associated with a higher overall survival rate in patients. These results provide mechanistic insight into the function of hCINAP during the DNA-damage response and its role in AML resistance to therapy." @default.
- W2959431180 created "2019-07-23" @default.
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- W2959431180 date "2019-08-23" @default.
- W2959431180 modified "2023-10-15" @default.
- W2959431180 title "hCINAP regulates the DNA-damage response and mediates the resistance of acute myelocytic leukemia cells to therapy" @default.
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- W2959431180 doi "https://doi.org/10.1038/s41467-019-11795-5" @default.
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