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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Journal ArticleDOI
Sestrin prevents atrophy of disused and aging muscles by integrating anabolic and catabolic signals
Jessica Segalés,Jessica Segalés,Eusebio Perdiguero,Antonio L. Serrano,Pedro Sousa-Victor,Pedro Sousa-Victor,Laura Ortet,Mercè Jardí,Andrei V. Budanov,Andrei V. Budanov,Laura García-Prat,Laura García-Prat,Laura García-Prat,Marco Sandri,David M. Thomson,Michael Karin,Jun Hee Lee,Pura Muñoz-Cánoves,Pura Muñoz-Cánoves +18 more
TL;DR: It is shown that expression of sestrins decreases during inactivity and that their overexpression prevents atrophy in mice via modulation of autophagy and protein degradation.
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Overexpressed human metallothionein IIA gene protects Chinese hamster ovary cells from killing by alkylating agents.
TL;DR: Results suggest that metallothionein participates as a cofactor or regulatory element in repair or tolerance of toxic alkylation lesions and free radicals generated by these agents cannot be scavenged efficiently by MT in vivo.
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Conditional ablation of Ikkb inhibits melanoma tumor development in mice
Jinming Yang,Ryan Splittgerber,Fiona E. Yull,Sara M. Kantrow,Gregory D. Ayers,Michael Karin,Ann Richmond +6 more
TL;DR: Results show that Ink4a/Arf-/- mice with melanocyte-specific deletion of Ikkb were protected from HRasV12-initiated melanoma only when p53 was expressed, providing genetic and mechanistic evidence that mutant HRas initiation of tumorigenesis requires Ikkbeta-mediated NF-kappaB activity.
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Growth hormone gene regulation: a paradigm for cell-type-specific gene activation.
TL;DR: The growth hormone (GH) gene is specifically expressed within specialized cells of the anterior pituitary, and the central role in GH gene activation is played by GHF-1, a homeodomain protein that is itself specifically expressed in the anterior Pituitary.
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Oxidized DNA fragments exit mitochondria via mPTP- and VDAC-dependent channels to activate NLRP3 inflammasome and interferon signaling.
Hongxu Xian,Kosuke Watari,Elsa Sanchez-Lopez,Joseph Offenberger,Janset Onyuru,Harini Sampath,Wei Ying,Hal M. Hoffman,Gerald S. Shadel,Michael Karin +9 more
TL;DR: In this article , the authors found that diverse NLRP3 inflammasome activators rapidly stimulated uniporter-mediated calcium uptake to open mitochondrial permeability transition pores (mPTP) and trigger VDAC oligomerization.