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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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Journal Article

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, +168 more
- 01 Jan 2018 - 
TL;DR: An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
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IKKβ Couples Hepatocyte Death to Cytokine-Driven Compensatory Proliferation that Promotes Chemical Hepatocarcinogenesis

TL;DR: IKKbeta orchestrates inflammatory crosstalk between hepatocytes and hematopoietic-derived cells that promotes chemical hepatocarcinogenesis and blocks excessive DEN-induced carcinogenesis in Ikkbeta(Deltahep) mice.
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p53 Target Genes Sestrin1 and Sestrin2 Connect Genotoxic Stress and mTOR Signaling

TL;DR: Sestrin1 and Sestrin2 provide an important link between genotoxic stress, p53 and the mTOR signaling pathway and are demonstrated to activate the AMP-responsive protein kinase (AMPK) and target it to phosphorylate TSC2 and stimulate its GAP activity, thereby inhibiting mTOR.
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How NF-kappaB is activated: the role of the IkappaB kinase (IKK) complex.

TL;DR: This review describes the identification of proteins in the IKK complex, and the regulation and physiological functions of IKK.
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Differential Activation of ERK and JNK Mitogen-Activated Protein Kinases by Raf-1 and MEKK

TL;DR: These results demonstrate the existence of two distinct Ras-dependent MAPK cascades--one initiated by Raf-1 leading to ERK activation, and the other initiated by MEKK leading to JNK activation.