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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The tumor promoter arsenite stimulates AP-1 activity by inhibiting a JNK phosphatase.
TL;DR: It is found that As3+, but not As5+, is a potent stimulator of AP‐1 transcriptional activity and an efficient inducer of c‐fos and c‐jun gene expression and the primary mechanism by which As3+ stimulates JNK activity involves the inhibition of a constitutive dual‐specificity JNK phosphatase.
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Loss of hepatic NF-κB activity enhances chemical hepatocarcinogenesis through sustained c-Jun N-terminal kinase 1 activation
TL;DR: It is suggested that the control of tissue renewal through the IKK and JNK pathways plays a key role in liver carcinogenesis.
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Identification of Liver Cancer Progenitors Whose Malignant Progression Depends on Autocrine IL-6 Signaling
Guobin He,Debanjan Dhar,Hayato Nakagawa,Hayato Nakagawa,Joan Font-Burgada,Hisanobu Ogata,Hisanobu Ogata,Yuhong Jiang,Shabnam Shalapour,Ekihiro Seki,Shawn Yost,Kristen Jepsen,Kelly A. Frazer,Olivier Harismendy,Maria Hatziapostolou,Dimitrios Iliopoulos,Atsushi Suetsugu,Robert M. Hoffman,Ryosuke Tateishi,Kazuhiko Koike,Michael Karin +20 more
TL;DR: In this article, the authors describe isolation and characterization of HCC progenitor cells (HcPCs) from different mouse HCC models and show that cells resembling HcPC cells reside within dysplastic lesions that appear several months before HCC nodules.
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JNK2 and IKKβ Are Required for Activating the Innate Response to Viral Infection
Wen Ming Chu,Derek Ostertag,Zhi-Wei Li,Lufen Chang,Yi Chen,Yinling Hu,Bryan R.G. Williams,Jacques Perrault,Michael Karin +8 more
TL;DR: A general role is established for IKKbeta and JNK2 are essential for efficient induction of type I IFN and other cytokines in response to viral infection or dsRNA and a pathway leading to NF-kappaB is described.
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From JNK to pay dirt: jun kinases, their biochemistry, physiology and clinical importance.
Michael Karin,Ewen Gallagher +1 more
TL;DR: The c‐Jun N‐terminal kinases (JNKs) were originally identified by their ability to phosphorylate c‐ Jun in response to UV‐irradiation, but now are recognized as critical regulators of various aspects of mammalian physiology, including: cell proliferation, cell survival, cell death, DNA repair and metabolism.