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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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The CUP2 gene product regulates the expression of the CUP1 gene, coding for yeast metallothionein.

TL;DR: CUP2, which is on chromosome VII, codes for or controls the synthesis or activity of a protein which binds the upstream control region of the CUP1 gene on chromosome VIII, establishing CUP2 as a regulatory gene for expression of theCUP1 metallothionein gene product.
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Liver Cancer Initiation Requires p53 Inhibition by CD44-Enhanced Growth Factor Signaling

TL;DR: CD44, a hyaluronic acid receptor whose expression is rapidly induced in carcinogen-exposed hepatocytes in a STAT3-dependent manner, allows DNA-damaged hepatocytes to escape p53-induced death and senescence and respond to proliferative signals that promote fixation of mutations and their transmission to daughter cells that go on to become HCC progenitors.
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Kinase regulation in inflammatory response

TL;DR: The transcription factor NF-κB is a pivotal regulator of innate immune responses, whose activity is rapidly induced by proinflammatory stimuli, most notably the tumour-necrosis factor TNFα and interleukin-1, viruses, and components of bacterial cell walls.
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The transactivating domain of the c-Jun proto-oncoprotein is required for cotransformation of rat embryo cells.

TL;DR: The studies indicate that there is a direct correlation between the ability of the c-Jun protein to activate transcription and cotransform rat embryo cells and the hypothesis that c- Jun transforms cells by stimulating the expression of transformation-mediating genes.
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An AMPK-caspase-6 axis controls liver damage in nonalcoholic steatohepatitis.

TL;DR: The AMPK–caspase-6 axis regulates liver damage in NASH, implicating AMPK and caspases-6 as therapeutic targets for the treatment of NASH.