M
Mingjia Tan
Researcher at University of Michigan
Publications - 42
Citations - 2366
Mingjia Tan is an academic researcher from University of Michigan. The author has contributed to research in topics: Ubiquitin ligase & Neddylation. The author has an hindex of 25, co-authored 40 publications receiving 2015 citations. Previous affiliations of Mingjia Tan include Pfizer & Parke-Davis.
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Journal ArticleDOI
Transcriptional Activation of the Human Glutathione Peroxidase Promoter by p53
TL;DR: This is the first report demonstrating that GPX is a novel p53 target gene, and the finding links the p53 tumor suppressor to an antioxidant enzyme and will facilitate study of the p 53 signaling pathway and antioxidant enzyme regulation.
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PTGF-β, a type β transforming growth factor (TGF-β) superfamily member, is a p53 target gene that inhibits tumor cell growth via TGF-β signaling pathway
TL;DR: PTGF-β, a secretory protein, is a p53 target that could mediate p53-induced growth suppression in autocrinal as well as paracrinal fashions and implied a potential important role of p53 in inflammation regulation via PTGF- β.
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A small molecule Smac-mimic compound induces apoptosis and sensitizes TRAIL- and etoposide-induced apoptosis in breast cancer cells
TL;DR: In these cell lines, Smac-mimic acts in an apparent IAPs dependent manner to induce apoptosis alone as well as sensitizes breast cancer cells to TRAIL or etoposide induced apoptosis via caspase-3 activation.
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APCCdc20 Suppresses Apoptosis through Targeting Bim for Ubiquitination and Destruction
Lixin Wan,Mingjia Tan,Jie Yang,Hiroyuki Inuzuka,Xiangpeng Dai,Tao Wu,Jia Liu,Jia Liu,Shavali Shaik,Guoan Chen,Jing Deng,Marcos Malumbres,Anthony Letai,Marc W. Kirschner,Yi Sun,Wenyi Wei +15 more
TL;DR: An important role for APC(Cdc20) in governing apoptosis is revealed, strengthening the rationale for developing specific Cdc20 inhibitors as effective anticancer agents.
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FBXW7 Facilitates Nonhomologous End-Joining via K63-Linked Polyubiquitylation of XRCC4.
TL;DR: It is shown that FBXW7 facilitates nonhomologous end-joining (NHEJ) repair and that FBxW7 depletion causes radiosensitization, and implies that inactivated FB XW7 in human cancers could be a strategy for increasing the efficacy of radiotherapy.