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
IKKβ Is Required for Prevention of Apoptosis Mediated by Cell-Bound but Not by Circulating TNFα
TL;DR: Using JNK-deficient mice, it is shown that JNK is required for ConA-induced liver damage and the antiapoptotic function of IKKβ, which is most critical in situations that involve cell-bound TNFα, is mediated partially through attenuation of JNK activity.
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p105 and p98 precursor proteins play an active role in NF-kappa B-mediated signal transduction.
TL;DR: It is demonstrated that the p105 and p98 precursors share functional properties with the I kappa B proteins, which also contain SWI6/ankyrin repeats, suggesting a second pathway leading to NF-kappa B induction, in which processing of the precursor rather than phosphorylation of I k Kappa B plays a major role.
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Sestrins orchestrate cellular metabolism to attenuate aging
TL;DR: This work has shown that inactivation of Sestrin genes in invertebrates resulted in diverse metabolic pathologies, including oxidative damage, fat accumulation, mitochondrial dysfunction, and muscle degeneration, that resemble accelerated tissue aging.
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Inflammation, Autophagy, and Obesity: Common Features in the Pathogenesis of Pancreatitis and Pancreatic Cancer
Ilya Gukovsky,Ilya Gukovsky,Ning Li,Jelena Todoric,Anna S. Gukovskaya,Anna S. Gukovskaya,Michael Karin +6 more
TL;DR: The roles of inflammation and autophagy, and their deregulation by obesity, in pancreatic diseases are reviewed and the connections among disordered pathways and important areas for future research are discussed.
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Sestrins Inhibit mTORC1 Kinase Activation through the GATOR Complex
Anita Parmigiani,Aida Nourbakhsh,Boxiao Ding,Wei Wang,Young Chul Kim,Konstantin Akopiants,Kun-Liang Guan,Michael Karin,Andrei V. Budanov +8 more
TL;DR: This work reports an AMPK-independent mechanism of mTORC1 inhibition by Sestrins mediated by their interaction with GATOR2, which is potentially involved in m TORC1 regulation by amino acids, rotenone, and tunicamycin, connecting stress response with mTORc1 inhibition.