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Wenjian Gan
Researcher at Beth Israel Deaconess Medical Center
Publications - 26
Citations - 2602
Wenjian Gan is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: PI3K/AKT/mTOR pathway & Protein kinase B. The author has an hindex of 21, co-authored 26 publications receiving 2057 citations. Previous affiliations of Wenjian Gan include Medical University of South Carolina & Peking University.
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Journal ArticleDOI
R-loop-mediated genomic instability is caused by impairment of replication fork progression
TL;DR: It is shown that R-loop formation induces chromosomal DNA rearrangements and recombination in Escherichia coli, just as it does in eukaryotes, and that this underlies the effects of R loops on genomic stability.
Journal ArticleDOI
PtdIns(3,4,5)P3-Dependent Activation of the mTORC2 Kinase Complex
Pengda Liu,Wenjian Gan,Y. Rebecca Chin,Kohei Ogura,Jianping Guo,Jinfang Zhang,Bin Wang,John Blenis,Lewis C. Cantley,Alex Toker,Bing Su,Bing Su,Wenyi Wei +12 more
TL;DR: This study unravels a PI3K-dependent mechanism for mTORC2 activation, allowing m TORC2 to activate AKT in a manner that is regulated temporally and spatially by PtdIns(3,4,5)P3.
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Cell-cycle-regulated activation of Akt kinase by phosphorylation at its carboxyl terminus
Pengda Liu,Michael J. Begley,Wojciech Michowski,Hiroyuki Inuzuka,Miriam Bracha Ginzberg,Daming Gao,Peiling Tsou,Wenjian Gan,Antonella Papa,Byeong Mo Kim,Lixin Wan,Amrik Singh,Bo Zhai,Min Yuan,Zhiwei Wang,Steven P. Gygi,Tae Ho Lee,Kun Ping Lu,Alex Toker,Pier Paolo Pandolfi,John M. Asara,Marc W. Kirschner,Piotr Sicinski,Lewis C. Cantley,Wenyi Wei +24 more
TL;DR: The results of this study show Akt S477/T479 phosphorylation to be an essential layer of the Akt activation mechanism to regulate its physiological functions, thereby providing a new mechanistic link between aberrant cell cycle progression and Akt hyperactivation in cancer.
Journal ArticleDOI
Sin1 phosphorylation impairs mTORC2 complex integrity and inhibits downstream Akt signalling to suppress tumorigenesis
Pengda Liu,Wenjian Gan,Hiroyuki Inuzuka,Adam S. Lazorchak,Daming Gao,Omotooke Arojo,Dou Liu,Lixin Wan,Bo Zhai,Yonghao Yu,Yonghao Yu,Min Yuan,Byeong Mo Kim,Shavali Shaik,Suchithra Menon,Steven P. Gygi,Tae Ho Lee,John M. Asara,Brendan D. Manning,John Blenis,Bing Su,Wenyi Wei +21 more
TL;DR: Results reveal a Sin1-phosphorylation-dependent mTORC2 regulation, providing a potential molecular mechanism by which mutations in the m TORC1–S6K–Sin1 signalling axis might cause aberrant hyper-activation of the mtorC2–Akt pathway, which facilitates tumorigenesis.
Journal ArticleDOI
Prostate cancer-associated SPOP mutations confer resistance to BET inhibitors through stabilization of BRD4.
Xiangpeng Dai,Wenjian Gan,Xiaoning Li,Xiaoning Li,Shangqian Wang,Wei Zhang,Ling Huang,Shengwu Liu,Qing Zhong,Jianping Guo,Jinfang Zhang,Ting Chen,Kouhei Shimizu,Francisco Beca,Mirjam Blattner,Divya Vasudevan,Dennis L. Buckley,Jun Qi,Lorenz Buser,Pengda Liu,Hiroyuki Inuzuka,Andrew H. Beck,Liewei Wang,Peter J. Wild,Levi A. Garraway,Mark A. Rubin,Christopher E. Barbieri,Kwok-Kin Wong,Senthil K. Muthuswamy,Jiaoti Huang,Yu Chen,James E. Bradner,Wenyi Wei +32 more
TL;DR: The results elucidate the tumor-suppressor role of SPOP in prostate cancer in which it acts as a negative regulator of BET protein stability and also provide a molecular mechanism for resistance to BET inhibitors in individuals with prostate cancer bearing SPOP mutations.