The metabolic function of cyclin D3–CDK6 kinase in cancer cell survival

被引：0
|
作者：
Haizhen Wang
Brandon N. Nicolay
Joel M. Chick
Xueliang Gao
Yan Geng
Hong Ren
Hui Gao
Guizhi Yang
Juliet A. Williams
Jan M. Suski
Mark A. Keibler
Ewa Sicinska
Ulrike Gerdemann
W. Nicholas Haining
Thomas M. Roberts
Kornelia Polyak
Steven P. Gygi
Nicholas J. Dyson
Piotr Sicinski
机构：
[1] Dana-Farber Cancer Institute,Department of Cancer Biology
[2] Harvard Medical School,Department of Genetics
[3] Massachusetts General Hospital Cancer Center,Department of Cell Biology
[4] Harvard Medical School,Department of Biological Chemistry and Molecular Pharmacology
[5] Harvard Medical School,Department of Chemical Engineering
[6] Novartis Institutes for Biomedical Research,Department of Oncologic Pathology
[7] Massachusetts Institute of Technology,Department of Pediatric Oncology
[8] Dana-Farber Cancer Institute,Division of Pediatric Hematology and Oncology
[9] Dana-Farber Cancer Institute,Department of Medical Oncology
[10] Children’s Hospital,undefined
[11] Broad Institute of MIT and Harvard,undefined
[12] Dana-Farber Cancer Institute,undefined
来源：
Nature | 2017年 / 546卷
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摘要：
The cyclin D3–CDK6 kinase complex, which is overactive in some cancers, inhibits two key glycolysis enzymes and thereby enhances the levels of antioxidants in cells, promoting tumour cell survival.
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页码：426 / 430
页数：4
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