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.
Papers
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Journal ArticleDOI
Shp2 deletion in hepatocytes suppresses hepatocarcinogenesis driven by oncogenic β-Catenin, PIK3CA and MET.
Jacey J. Liu,Yanjie Li,Yanjie Li,Wendy S. Chen,Yan Liang,Gaowei Wang,Min Zong,Kota Kaneko,Ruiyun Xu,Michael Karin,Gen-Sheng Feng +10 more
TL;DR: It is shown that a cytoplasmic tyrosine phosphatase Shp2 is required for liver tumorigenesis, which is driven by two oncoproteins that are implicated in human liver cancer.
Book ChapterDOI
Tissue-specific expression of the growth hormone gene and its control by growth hormone factor-1.
TL;DR: This chapter discusses the tissue-specific expression of the growth hormone gene and its control by growth hormone, and discusses various features of GHF-1, which has a novel type of activation domain that interacts with the components of the transcriptional machinery.
Journal ArticleDOI
The MEKK1 PHD ubiquitinates TAB1 to activate MAPKs in response to cytokines
TL;DR: Map3k1mPHD ES cells demonstrate that the MEKK1 PHD controls p38 and JNK activation during TGF‐β, EGF and microtubule disruption signalling, but does not affect MAPK responses to hyperosmotic stress.
Journal Article
IkappaB kinase alpha is essential for development of the mammalian cornea and conjunctiva.
TL;DR: IKKalpha is specifically required for formation of cornea and conjunctiva and this function may be exerted through an effect on NF-kappaB activity.
Journal ArticleDOI
Recent Insights Into the Pathogenic Mechanism of Pancreatitis: Role of Acinar Cell Organelle Disorders.
Anna S. Gukovskaya,Fred S. Gorelick,Guy E. Groblewski,Olga A. Mareninova,Aurelia Lugea,Laura Antonucci,Richard T. Waldron,Aida Habtezion,Michael Karin,Stephen J. Pandol,Ilya Gukovsky +10 more
TL;DR: Studies in experimental and genetic AP models show that acinar cell injury is mediated by distinct mechanisms of organelle dysfunction involved in protein synthesis and trafficking, secretion, energy generation, and autophagy, and suggest that targeting specific mediators ofOrganelle dysfunction could reduce disease severity.