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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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IκB kinase α kinase activity is required for self-renewal of ErbB2/Her2-transformed mammary tumor-initiating cells

TL;DR: Strikingly, primary IkkαAA/AA/MMTV-c-neu carcinoma cells exhibited diminished self-renewal capacity, resulting in the inability to establish secondary tumors, suggesting IKKα may represent a novel and specific target for treatment of ErbB2-positive breast cancer.
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Too many transcription factors: positive and negative interactions.

TL;DR: The examples described here illustrate an emerging new mode of cellular regulation mediated by closely related but functionally distinct transcription factors that appear to compete for common binding sites.
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AP-1--glucocorticoid receptor crosstalk taken to a higher level.

TL;DR: It has become clear that negative crosstalk between the GC receptor (GCR) and transcription factor AP-1 (Jun:Fos) underlie the anti-inflammatory and immunosuppressive activity of GC.
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Oxidative stress and gene expression: The AP-1 and NF-κB connections

TL;DR: Two transcription factors, NF-κB and AP-1, have emerged in recent years as major targets for signaling pathways that are activated by a variety of proinflammatory stimuli and their regulation by oxidative stress and pro-oxidants will be addressed.
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Role of microglial IKKβ in kainic acid-induced hippocampal neuronal cell death

TL;DR: In this paper, the IKK/nuclear factor-κB dependent microglia activation contributes to KA-induced hippocampal neuronal cell death in vivo through induction of inflammatory mediators.