双重准SLC25A51和酸脱酶可以选择性地耗尽线粒体NAD,以消除KRAS驱动的AML

Ang Jia1, Xiaowen Zhang2, Ji-Hao Zhou3

  • 1Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Drug Clinical Trial Center, Shanghai Xuhui Central Hospital, Zhongshan-Xuhui Hospital, Fudan University, Institute of Clinical Mass Spectrometry, Shanghai Academy of Experimental Medicine, Shanghai, China; State Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.

Cell metabolism
|January 30, 2026
PubMed
概括

新的研究确定了基尔斯大鼠肉瘤病毒性瘤基因同类 (KRAS) 突变作为激进的急性髓性白血病 (AML) 的关键驱动因素. 一种新型的双重向化合物通过破坏线粒体NAD+代谢来选择性地消除KRAS突变AML细胞.

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