一个致瘤性的琥珀酰化开关：SUCLG1、线粒体转录和白血病。
A succinylation switch to maligancy: SUCLG1, mitochondrial transcription and leukemia.
机构信息
Leukemia Therapy Resistance Unit, Department of Biomolecular Medicine, Ghent University, Ghent, Belgium.
Center for Medical Genetics, Ghent University and University Hospital, Ghent, Belgium.
出版信息
EMBO J. 2024 Jun;43(12):2291-2293. doi: 10.1038/s44318-024-00116-2. Epub 2024 May 9.
Abstract
The cellular consequences of activating FLT3 mutations in blood cancers are poorly understood. In this issue, Yan et al (2024) demonstrate that FLT3 activation promotes mitobiogenesis and leukemia progression through a posttranslational control mechanism, linking cell metabolism with derepressed mitochondrial transcription and function.
摘要
激活血液癌症中的 FLT3 突变的细胞后果知之甚少。在本期杂志中，Yan 等人（2024 年）证明，FLT3 的激活通过一种翻译后控制机制促进了有丝分裂发生和白血病进展，将细胞代谢与去抑制的线粒体转录和功能联系起来。
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