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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Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor.
Peter Angel,Masayoshi Imagawa,Robert Chiu,Bernd Stein,Richard J. Imbra,Hans J. Rahmsdorf,Carsten Jonat,Peter Herrlich,Michael Karin +8 more
TL;DR: Results strongly suggest that AP-1 is at the receiving end of a complex pathway responsible for transmitting the effects of phorbol ester tumor promoters from the plasma membrane to the transcriptional machinery.
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NF-kappaB: linking inflammation and immunity to cancer development and progression.
Michael Karin,Florian R. Greten +1 more
TL;DR: The hypothesis is put forward that activation of nuclear factor-κB by the classical, IKK-β (inhibitor-of-NF-β kinase-β)-dependent pathway is a crucial mediator of inflammation-induced tumour growth and progression, as well as an important modulator of tumour surveillance and rejection.
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AP-1 as a regulator of cell life and death
Eitan Shaulian,Michael Karin +1 more
TL;DR: Interestingly, the growth-promoting activity of c-Jun is mediated by repression of tumour suppressors, as well as upregulation of positive cell cycle regulators, whereas JunB has the converse effect.
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NF-κB at the crossroads of life and death
Michael Karin,Anning Lin +1 more
TL;DR: The choice between life and death is one of the major events in regulation of the immune system and a major regulator of such life or death decisions is the transcription factor NF-κB as mentioned in this paper.
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The Regulation of AP-1 Activity by Mitogen-activated Protein Kinases
TL;DR: The specific roles of three MAPKs, namely ERK, JNK and FRK, in modulation of both the level and activity of AP-1, are discussed.