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
p38-dependent phosphorylation of the mRNA decay-promoting factor KSRP controls the stability of select myogenic transcripts.
Paola Briata,Sonia Vanina Forcales,Marco Ponassi,Giorgio Corte,Ching Yi Chen,Michael Karin,Pier Lorenzo Puri,Roberto Gherzi +7 more
TL;DR: It is demonstrated that p38 alpha and beta isoforms also control muscle-gene expression posttranscriptionally, by stabilizing critical myogenic transcripts, by establishing a biochemical link between differentiation-activated p38 signaling and turnover of myogenic mRNAs.
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Saturated Fatty Acids Induce c-Src Clustering within Membrane Subdomains, Leading to JNK Activation
Ryan G. Holzer,EekJoong Park,Ning Li,Helen Tran,Monica Chen,Crystal Choi,Giovanni Solinas,Michael Karin +7 more
TL;DR: It is demonstrated that saturated FA activate JNK and inhibit insulin signaling through c-Src activation, which is more likely to cause insulin resistance and type 2 diabetes than unsaturated FA.
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Immunity by ubiquitylation: a reversible process of modification
TL;DR: This Review covers recent progress in the understanding of protein ubiquitylation in the immune system, and the conjugation of ubiquitin-like molecules, such as ISG15, to proteins is also involved in immune regulation.
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Signal transduction from cell surface to nucleus in development and disease.
TL;DR: This review discusses the basic outline of the eukaryotic signal transduction systems used to transmit information from the cell surface to the transcriptional machinery in the nucleus.
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The IkappaB kinase - a bridge between inflammation and cancer.
TL;DR: In this paper, the authors proposed that NF-kappaB transcription factors regulated via the IkappaB kinase (IKK) complex play a critical role in coupling inflammation and cancer and set out to test this hypothesis in mouse models of cancer.