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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Molecular mechanisms of immunosuppression and anti-inflammatory activities by glucocorticoids.
TL;DR: The purpose of the review is to describe the molecular mechanisms that may account for the potent repressiveeffects of OCs on genes that are activated by transcription factors AP-I and NF-KB.
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Biphasic increase in c-jun mRNA is required for induction of AP-1-mediated gene transcription: differential effects of muscarinic and thrombin receptor activation.
TL;DR: It is suggested that rapid and transient conduction of c-fos and c-jun mRNA is insufficient to induce prominent changes in gene transcription, while the sustained increase in c-Jun mRNA and perhaps the late induction of fra-1 mRNA are required for generation of AP-1 DNA-binding activity and transactivation throughAP-1.
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Extinction of growth hormone expression in somatic cell hybrids involves repression of the specific trans-activator GHF-1
Alison McCormick,David J. Wu,José-Luis Castrillo,Sharon Dana,Jeannine S. Strobl,E. Brad Thompson,Michael Karin +6 more
TL;DR: Describing two parental cell lines and three hybrids suggested that extinction of GH expression in fibroblast x pituitary hybrids was accompanied by loss of GHF-1 protein and mRNA expression, suggesting that extinction occurs by repression of this trans-activator.
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M-phase-specific phosphorylation of the POU transcription factor GHF-1 by a cell cycle-regulated protein kinase inhibits DNA binding.
TL;DR: Thr-220 of GHF-1 is the homolog of the mitotic phosphoacceptor site responsible for the M-phase-specific inhibition of Oct-1 DNA binding Ser-382, which appears to be involved in regulating the DNA binding activity of all POU proteins in a cell cycle-dependent manner.
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The wild-derived inbred mouse strain SPRET/Ei is resistant to LPS and defective in IFN-beta production.
Tina Mahieu,Jin Mo Park,Hilde Revets,Bastian Pasche,Andreas Lengeling,Jan Staelens,Andy Wullaert,Ineke Vanlaere,Tino Hochepied,Frans van Roy,Michael Karin,Claude Libert +11 more
TL;DR: It is demonstrated that SPRET/Ei mice, derived from Mus spretus, exhibit a dominant resistance against LPS-induced lethality, mediated by bone marrow-derived cells and disruption of a positive-feedback loop that amplifies IFN-β production.