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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IL-1β-driven neutrophilia preserves antibacterial defense in the absence of the kinase IKKβ.
Li-Chung Hsu,Li-Chung Hsu,Thomas Enzler,Thomas Enzler,Jun Seita,Anjuli M. Timmer,Chih-Yuan Lee,Ting-Yu Lai,Guann-Yi Yu,Liang-Chuan Lai,Vladislav Temkin,Ursula Sinzig,Thiha Aung,Victor Nizet,Victor Nizet,Irving L. Weissman,Michael Karin +16 more
TL;DR: In this article, the authors found neutrophilia in mice with inducible deletion of IKKβ (Ikkβ(Δ) mice) and showed that deletion of interleukin 1 receptor 1 (IL-1R1) normalized blood cellularity and prevented neutrophil-driven inflammation.
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Inflammation and cancer: the long reach of Ras.
TL;DR: Insights now emerge from work on Ras and the proinflammatory mediator interleukin-8, produced by tumor-infiltrating immune cells, and the role they play in tumor growth and survival.
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Molecular cloning and characterization of a novel Rel/NF-kappa B family member displaying structural and functional homology to NF-kappa B p50/p105.
TL;DR: The NF-χB transcription factor consists of two subunits that are implicated in the inducible expression of many genes, including inflammatory, immune, and acute-phase response genes.
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From death receptor to reactive oxygen species and c‐Jun N‐terminal protein kinase: the receptor‐interacting protein 1 odyssey
Vladislav Temkin,Michael Karin +1 more
TL;DR: Death receptors are more than simple killers: they control cell growth, proliferation, and survival, thereby playing a pivotal role in immune and inflammatory responses, and these molecular mechanisms may be involved in neoplastic, autoimmune, neurodegenerative, inflammatory, and metabolic diseases.
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Intestinal glucuronidation protects against chemotherapy-induced toxicity by irinotecan (CPT-11)
Shujuan Chen,Mei-Fei Yueh,Cyril Bigo,Olivier Barbier,Kepeng Wang,Michael Karin,Nghia Nguyen,Robert H. Tukey +7 more
TL;DR: By selectively targeting the deletion of the Ugt1 locus in either liver or intestinal tissue, it is confirmed that intestinal UGT1A-specific glucuronidation ofSN-38 is essential in preventing SN-38–induced toxicity, and being able to induce intestinal U GT1A1 may be effective in reducing CPT-11 toxicity.