DNMT3A 突变造血干细胞重编程 IFNγ 信号获得克隆优势。
Dnmt3a-Mutant Hematopoietic Stem Cell Rewire IFNγ Signaling to Gain Clonal Advantage.
机构信息
Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
出版信息
Blood Cancer Discov. 2022 May 5;3(3):178-180. doi: 10.1158/2643-3230.BCD-22-0025.
Abstract
Dnmt3a-mutant stem cells gain a competitive advantage via upregulation of a Txnip-p53-p21 axis and protection from IFNγ induced exhaustion. See related article by Zhang et al., p. 220 (5).
摘要
DNMT3A 突变的干细胞通过上调 TXNIP-p53-p21 轴获得竞争优势，并免受 IFNγ 诱导的衰竭。见张等相关文章，第 220 页（5）。
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本文引用的文献
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Hotspot DNMT3A mutations in clonal hematopoiesis and acute myeloid leukemia sensitize cells to azacytidine via viral mimicry response.热点 DNMT3A 突变在克隆性造血和急性髓系白血病中通过病毒模拟反应使细胞对阿扎胞苷敏感。
Nat Cancer. 2021 May;2(5):527-544. doi: 10.1038/s43018-021-00213-9. Epub 2021 May 25.
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Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling.慢性感染通过 IFNγ 信号通路驱动 Dnmt3a 功能丧失性克隆性造血。
Cell Stem Cell. 2021 Aug 5;28(8):1428-1442.e6. doi: 10.1016/j.stem.2021.03.002. Epub 2021 Mar 19.
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