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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 Article

The IL-23 to IL-17 cascade inflammation-related cancers.

TL;DR: Findings suggest that IL-23 and/or IL-17A inhibitors should be evaluated for their therapeutic and preventative potential in human cancers, especially in colorectal cancer.
Journal ArticleDOI

IKKα Is a p63 Transcriptional Target Involved in the Pathogenesis of Ectodermal Dysplasias

TL;DR: The data demonstrate that a failure to properly express IKKalpha may play a role in the development of ectodermal dysplasias and identify I-kappaB kinase alpha (IKKalpha) as a direct transcriptional target of p63 that is induced at early phases of terminal differentiation of primary keratinocytes.
Journal ArticleDOI

Epithelial Cell IκB-Kinase β Has an Important Protective Role in Clostridium difficile Toxin A-Induced Mucosal Injury

TL;DR: It is concluded that activation of intestinal epithelial cell NF-κB by toxin A plays an important host mucosal protective role after C. difficile toxin A exposure that is mediated, at least in part, through promoting epithelialcell survival by abrogating epithel cell apoptosis.
Journal ArticleDOI

Obesity, autophagy and the pathogenesis of liver and pancreatic cancers

TL;DR: The relationships between autophagy, nuclear factor‐κB signaling and obesity in hepatocellular carcinoma will be discussed, as well as the dual role of Autophagy in pancreatic ductal adenocarcinoma.
Book ChapterDOI

Signaling pathways leading to nuclear factor-kappa B activation.

TL;DR: This chapter focuses on studying signaling pathways triggered by a stimulus (e.g., UVA) that ultimately lead to NF-KB activation.