CDK5-dependent phosphorylation and nuclear translocation of TRIM59 promotes macroH2A1 ubiquitination and tumorigenicity

Youzhou Sang; Yanxin Li; Yingwen Zhang; Angel A. Alvarez; Bo Yu; Weiwei Zhang; Bo Hu; Shi-Yuan Cheng; Haizhong Feng

doi:10.1038/s41467-019-12001-2

Nature Communications (Sep 2019)

CDK5-dependent phosphorylation and nuclear translocation of TRIM59 promotes macroH2A1 ubiquitination and tumorigenicity

Youzhou Sang,
Yanxin Li,
Yingwen Zhang,
Angel A. Alvarez,
Bo Yu,
Weiwei Zhang,
Bo Hu,
Shi-Yuan Cheng,
Haizhong Feng

Affiliations

Youzhou Sang: State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, Shanghai Jiao Tong University
Yanxin Li: Key Laboratory of Pediatric Hematology and Oncology Ministry of Health, Pediatric Translational Medicine Institute, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University
Yingwen Zhang: Key Laboratory of Pediatric Hematology and Oncology Ministry of Health, Pediatric Translational Medicine Institute, Shanghai Children’s Medical Center, School of Medicine, Shanghai Jiao Tong University
Angel A. Alvarez: The Ken and Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine
Bo Yu: State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, Shanghai Jiao Tong University
Weiwei Zhang: State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, Shanghai Jiao Tong University
Bo Hu: The Ken and Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine
Shi-Yuan Cheng: The Ken and Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine
Haizhong Feng: State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, School of Medicine, Shanghai Jiao Tong University

DOI: https://doi.org/10.1038/s41467-019-12001-2
Journal volume & issue: Vol. 10, no. 1
pp. 1 – 17

Abstract

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CDK5 is known to drive glioblastoma tumorigenicity but the downstream molecular mechanism is unknown. Here, the authors show that CDK5 activates STAT3 signalling via the nuclear import of TRIM59, which leads to the degradation of the tumour suppressor macroH2A1.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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