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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.

Papers
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Patent

Methods for identifying and using IKK inhibitors

TL;DR: In this paper, the authors provide methods and compositions for inhibiting IKK and COX2, as well as identifying compounds with activity as inhibitors of IKK, and for the treatment of diseases and conditions wherein IKK is implicated and inhibition of its activity is desired.
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Inactivation of IκB-kinase-β dependent genes in airway epithelium reduces tobacco smoke induced acute airway inflammation

TL;DR: An important role for NF-kappaB regulated genes in airway epithelium in contributing to acute tobacco smoke induced airway inflammation not only in the peribronchial space but also in the alveolar space is demonstrated.
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Signaling cascades and inflammasome activationin microbial infections

TL;DR: This review analyzes the current knowledge regarding association of innate immune signaling pathways with inflammasome activation in response to bacterial infection and recognizes recognition of extracellular pathogenassociated molecular patterns by pattern recognition receptors (PRRs) results in activation of host defense signaling pathways.
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Intermittent hypoxia and hypercapnia induces inhibitor of nuclear factor-κB kinase subunit β-dependent atherosclerosis in pulmonary arteries.

TL;DR: IKKβ-dependent NF-kappa B activity in myeloid-lineage cells plays a critical role in IHH-induced PA atherosclerosis at the early stage, and both IKKβ deletion and IHH have no effects on Atherosclerosis in the aorta.
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IκB kinase β (IKKβ) does not mediate feedback inhibition of the insulin signalling cascade.

TL;DR: The findings that IKKβ, although activated by insulin, does not promote direct serine phosphorylation of IRS1 and does not contribute to the feedback inhibition of the insulin signalling cascade are confirmed.