M
Michael Karin
Researcher at University of California, San Diego
Publications - 753
Citations - 246120
Michael Karin is an academic researcher from University of California, San Diego. The author has contributed to research in topics: IκB kinase & Signal transduction. The author has an hindex of 236, co-authored 704 publications receiving 226485 citations. Previous affiliations of Michael Karin include Sanford-Burnham Institute for Medical Research & University of California, Los Angeles.
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Journal ArticleDOI
TANK-binding kinase 1 (TBK1) controls cell survival through PAI-2/serpinB2 and transglutaminase 2
Mireille Delhase,Soo-Youl Kim,Ho Lee,Aya Naiki-Ito,Yi Chen,Eu-Ree Ahn,Kazuhiro Murata,Se-Jin Kim,Norman Lautsch,Koichi Kobayashi,Tomoyuki Shirai,Michael Karin,Makoto Nakanishi +12 more
TL;DR: It is shown that TBK1 triggers an antiapoptotic response by controlling a specific RelA/p65 phosphorylation event, which results in inducible expression of plasminogen activator inhibitor-2 (PAI-2) and transglutaminase 2 (TG2), which cross-links and inactivates procaspase-3.
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Ikappa B kinaseβ/nuclear factor‐κB activation controls the development of liver metastasis by way of interleukin‐6 expression
Shin Maeda,Yohko Hikiba,Kei Sakamoto,Hayato Nakagawa,Yoshihiro Hirata,Yoku Hayakawa,Ayako Yanai,Keiji Ogura,Michael Karin,Masao Omata +9 more
TL;DR: Observations suggest that IKKβ/NF‐κB activation controls the development of liver metastasis by way of IL‐6 expression and is a potential target for theDevelopment of antimetastatic drugs.
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Analysis of nondegradative protein ubiquitylation with a monoclonal antibody specific for lysine-63-linked polyubiquitin
Haopeng Wang,Atsushi Matsuzawa,Scott A. Brown,Jingran Zhou,Cliff Guy,Ping Hui Tseng,Karen Forbes,Thomas P. Nicholson,Paul W. Sheppard,Hans Häcker,Michael Karin,Dario A. A. Vignali +11 more
TL;DR: This work has generated a monoclonal antibody (mAb) that specifically recognizes K63-linked polyUb, but not any other isopeptide-linked (K6, K11, K27, K29, K33, or K48) polyUb or monoubiquitin.
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Sestrins are evolutionarily conserved mediators of exercise benefits
Myungjin Kim,Alyson Sujkowski,Sim Namkoong,Sim Namkoong,Bondong Gu,Tyler Cobb,Boyoung Kim,Allison H. Kowalsky,Chun-Seok Cho,Ian A. Semple,Seung-Hyun Ro,Seung-Hyun Ro,Carol S. Davis,Susan V. Brooks,Michael Karin,Robert Wessells,Jun Hee Lee +16 more
TL;DR: It is identified that Sestrins, proteins induced by exercise, are key mediators of the metabolic adaptation to exercise and increase endurance through the AKT and PGC1a axes.
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Mitogen activated protein kinases as targets for development of novel anti-inflammatory drugs.
TL;DR: The pros and cons of targeting MAPKs in the treatment of chronic inflammatory disease are discussed and the possible mechanisms through which such inhibitors may interfere with inflammation are discussed.