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
Is NF-κB a good target for cancer therapy? Hopes and pitfalls
Véronique Baud,Michael Karin +1 more
TL;DR: Recent evidence from cancer genetics and cancer genome studies that support the involvement of NF-κB in human cancer, particularly in multiple myeloma are discussed.
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Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer
TL;DR: Despite these versatile and occasionally antagonistic interactions, NF-kappaB and STAT3 cooperate to promote the development and progression of colon, gastric and liver cancers and offer opportunities for the design of new therapeutic interventions.
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Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6
Hans Häcker,Vanessa Redecke,Blagoy Blagoev,Irina Kratchmarova,Li-Chung Hsu,Gang Greg Wang,Mark P. Kamps,Eyal Raz,Hermann Wagner,Georg Häcker,Matthias Mann,Michael Karin +11 more
TL;DR: It is shown that TRAF3 is essential for the induction of type I interferons (IFN) and the anti-inflammatory cytokine interleukin-10 (IL-10), but is dispensable for expression of pro- inflammatory cytokines, owing to defective IL-10 production.
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JNK is involved in signal integration during costimulation of T lymphocytes
TL;DR: In this article, the authors investigated the effect of phorbol ester and Ca2+ ionophore stimuli on mitogen activated protein (MAP) kinases and found that activation of the MAP kinases that phosphorylate the Jun activation domain, JNK1 and JNK2, required costimulation of T cells with either TPA and Ca 2+ ionsophore or antibodies to TCR and CD28.
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The IKKβ Subunit of IκB Kinase (IKK) is Essential for Nuclear Factor κB Activation and Prevention of Apoptosis
Zhi-Wei Li,Wen Ming Chu,Yinling Hu,Mireille Delhase,T. J. Deerinck,Mark H. Ellisman,Randall S. Johnson,Michael Karin +7 more
TL;DR: IKKβ-deficient mice are defective in activation of IKK and NF-κB in response to either tumor necrosis factor α or interleukin 1, and IKKα is unresponsive to IKK activators.