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突变的代谢重编程与易损性

The metabolic reprogramming and vulnerability of mutations.

作者信息

Dalton W Brian

机构信息

Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.

出版信息

Mol Cell Oncol. 2020 Feb 16;7(3):1697619. doi: 10.1080/23723556.2019.1697619. eCollection 2020.

DOI:10.1080/23723556.2019.1697619
PMID:32391415
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7199762/
Abstract

Mutations in the splicing factor 3b subunit 1 () gene create a neomorphic protein that disrupts RNA splicing, but the downstream consequences of this missplicing are unclear. Our recent study of isogenic human cells demonstrated that induces reprogramming of energy metabolism and a targetable vulnerability to deprivation of the nonessential amino acid serine.

摘要

剪接因子3b亚基1（）基因的突变产生一种新形态蛋白，该蛋白会破坏RNA剪接，但这种错误剪接的下游后果尚不清楚。我们最近对同基因人类细胞的研究表明，会诱导能量代谢重编程以及对非必需氨基酸丝氨酸剥夺产生可靶向的脆弱性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6548/7199762/ec6d1ba33e92/kmco-07-03-1697619-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6548/7199762/ec6d1ba33e92/kmco-07-03-1697619-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6548/7199762/ec6d1ba33e92/kmco-07-03-1697619-g001.jpg

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本文引用的文献

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J Clin Invest. 2019 Aug 8;129(11):4708-4723. doi: 10.1172/JCI125022.
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Reprogramming identifies functionally distinct stages of clonal evolution in myelodysplastic syndromes.重编程鉴定出骨髓增生异常综合征中克隆进化的功能不同阶段。
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Multiple enzymatic defects in mitochondria in hematological cells of patients with primary sideroblastic anemia.原发性铁粒幼细胞贫血患者血液学细胞线粒体中的多种酶缺陷。
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