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
ER Stress Drives Lipogenesis and Steatohepatitis via Caspase-2 Activation of S1P
Ju Youn Kim,Ricard Garcia-Carbonell,Shinichiro Yamachika,Peng Zhao,Debanjan Dhar,Rohit Loomba,Randal J. Kaufman,Alan R. Saltiel,Michael Karin +8 more
TL;DR: It is shown that caspase-2, whose expression is ER-stress inducible and elevated in human and mouse NASH, controls the buildup of hepatic-free cholesterol and triglycerides by activating sterol regulatory element-binding proteins (SREBP) in a manner refractory to feedback inhibition.
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Stressin' Sestrins take an aging fight
TL;DR: Sestrins are a family of highly conserved stress‐responsive proteins, transcriptionally regulated by p53 and forkhead transcription factor that exhibit oxidoreductase activity in vitro and can protect cells from oxidative stress.
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NOD2 contributes to cutaneous defense against Staphylococcus aureus through α-toxin-dependent innate immune activation
Petr Hruz,Annelies S. Zinkernagel,Gabriela Jenikova,Gregory J. Botwin,Jean-Pierre Hugot,Michael Karin,Victor Nizet,Victor Nizet,Lars Eckmann +8 more
TL;DR: It is shown that NOD2-deficient mice exhibit a delayed but ultimately exacerbated ulcerative response and impaired bacterial clearance after s.c. infection with S. aureus and it is demonstrated that this microbial sensor contributes to the discrimination between commensal bacteria and bacterial pathogens that elaborate pore-forming toxins.
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An antiinflammatory role for IKKβ through the inhibition of "classical" macrophage activation
Carol Ho Yan Fong,Magali Bebien,Arnaud Didierlaurent,Ruth Nebauer,Tracy Hussell,David H. Broide,Michael Karin,Toby Lawrence +7 more
TL;DR: It is suggested that IKKβ inhibits the “classically” activated or M1 macrophage phenotype during infection through negative cross talk with the Stat1 pathway, which may represent a mechanism to prevent the over-exuberant activation of macrophages during infection and contribute to the resolution of inflammation.
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Nuclear Export of NF90 Is Required for Interleukin-2 mRNA Stabilization
TL;DR: NF90, a previously described RNA binding protein, binds to a subregion of the 3'UTR that contains several AREs and slows down the degradation of IL-2 mRNA.