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
Convergence of Itch-induced ubiquitination with MEKK1-JNK signaling in Th2 tolerance and airway inflammation.
K. Venuprasad,Chris Elly,Min Gao,Shahram Salek-Ardakani,Yohsuke Harada,Jun-Li Luo,Chun Yang,Michael Croft,Kazushi Inoue,Michael Karin,Yun-Cai Liu +10 more
TL;DR: It is suggested that MEKK1-JNK signaling regulates Itch E3 ligase-mediated tolerogenic process in Th2 cells, which has therapeutic implications for allergic diseases.
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Isolation of a cDNA encoding a metal response element binding protein using a novel expression cloning procedure: the one hybrid system.
TL;DR: This work has used the one-hybrid system to isolate a mammalian cDNA clone encoding a sequence-specific DNA-binding protein that recognizes the metal response elements (MREs) of the metallothionein genes.
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p62/SQSTM1—Dr. Jekyll and Mr. Hyde that prevents oxidative stress but promotes liver cancer
TL;DR: This review discusses p62‐mediated signaling pathways and their roles in liver pathophysiology, especially NASH and HCC, where p62 elevation contributes to HCC development by preventing oncogene‐induced senescence and death of cancer‐initiating cells and enhancing their proliferation.
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Altering the specificity of signal transduction cascades: positive regulation of c-Jun transcriptional activity by protein kinase A.
TL;DR: Positive and conclusive proof that phosphorylation of c‐Jun on a critical site (Ser73) located in its activation domain is directly responsible for enhancing its transactivation function is provided.
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Stress-Activated NRF2-MDM2 Cascade Controls Neoplastic Progression in Pancreas
Jelena Todoric,Jelena Todoric,Laura Antonucci,Giuseppe Di Caro,Ning Li,Xuefeng Wu,Nikki K. Lytle,Debanjan Dhar,Sourav Banerjee,Johan Bourghardt Fagman,Cecille D. Browne,Atsushi Umemura,Atsushi Umemura,Mark A. Valasek,Hannes Kessler,David Tarin,Michael Goggins,Tannishtha Reya,Maria T. Diaz-Meco,Jorge Moscat,Michael Karin +20 more
TL;DR: It is shown that accumulation of the autophagy substrate p62/SQSTM1 in stressed KrasG12D acinar cells is associated with PDAC development and maintenance of malignancy in human cells and mice and that MDM2 targeting may be useful for preventingPDAC development in high-risk individuals.