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
YAP–IL-6ST autoregulatory loop activated on APC loss controls colonic tumorigenesis
Koji Taniguchi,Koji Taniguchi,Koji Taniguchi,Toshiro Moroishi,Petrus R. de Jong,Petrus R. de Jong,Michal Krawczyk,Britta Moyo Grebbin,Britta Moyo Grebbin,Huiyan Luo,Huiyan Luo,Rui-Hua Xu,Nicole Golob-Schwarzl,Caroline Schweiger,Kepeng Wang,Kepeng Wang,Giuseppe Di Caro,Ying Feng,Eric R. Fearon,Eyal Raz,Lukas Kenner,Lukas Kenner,Henner F. Farin,Henner F. Farin,Kun-Liang Guan,Johannes Haybaeck,Johannes Haybaeck,Christian Datz,Kang Zhang,Michael Karin +29 more
TL;DR: It is found that loss of adenomatous polyposis coli (APC) results in up-regulation of IL-6 signal transducer (IL-6ST/gp130), thereby activating Src family kinases (SFKs), YAP, and STAT3, which are simultaneously up-regulated in the majority of human CRC.
Journal ArticleDOI
NF-κB Activation in Hypothalamic Pro-opiomelanocortin Neurons Is Essential in Illness- and Leptin-induced Anorexia
Pil Geum Jang,Cherl Namkoong,Gil Myoung Kang,Man-Wook Hur,Seung-Whan Kim,Geun Hyang Kim,Yeoungsup Kang,Min Jae Jeon,Eunhee Kim,Myung-Shik Lee,Michael Karin,Ja Hyun Baik,Joong Yeol Park,Ki Up Lee,Young-Bum Kim,Min Seon Kim +15 more
TL;DR: In animal models of infection-associated anorexia, hypothalamic NF-κB was activated by leptin, an important anorexigenic hormone, and mediates leptin-stimulated POMC transcription, indicating that hypothalamicNF-κBs also serves as a downstream signaling pathway of leptin.
Journal Article
Elevation of AP1 activity during F9 cell differentiation is due to increased c-jun transcription.
Yang-Yen Hf,Chiu R,Michael Karin +2 more
TL;DR: The results demonstrate that AP1 activity can be stimulated by phorbol ester without concomitant c-fos induction, and indicates that, in the absence of c-Fos, only c-Jun is an effective transactivator.
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Antiinflammatory functions of p38 in mouse models of rheumatoid arthritis: advantages of targeting upstream kinases MKK-3 or MKK-6.
Monica Guma,Deepa Hammaker,Katharyn Topolewski,Maripat Corr,David L. Boyle,Michael Karin,Gary S. Firestein +6 more
TL;DR: Inhibiting p38α in a disease that is dominated by macrophage cytokines, such as RA, could paradoxically suppress antiinflammatory functions and interfere with clinical efficacy.
Journal ArticleDOI
Synergistic interaction of MEK kinase 2, c-Jun N-terminal kinase (JNK) kinase 2, and JNK1 results in efficient and specific JNK1 activation.
TL;DR: Investigating the molecular basis of activation of the c-Jun N-terminal kinase (JNK) subgroup of MAPK by the MAPKKK MEKK2 found that strong and specific JNK1 activation byMEKK2 was mediated by theMAPKK JNK kinase 2 (JNKK2) rather than by JNKK1 through formation of a tripartite complex consisting of MEKK 2, JNkk2, andJNK1.