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Benoit Dérijard

Researcher at University of Nice Sophia Antipolis

Publications -  35
Citations -  14744

Benoit Dérijard is an academic researcher from University of Nice Sophia Antipolis. The author has contributed to research in topics: Mitogen-activated protein kinase & Signal transduction. The author has an hindex of 24, co-authored 35 publications receiving 14509 citations. Previous affiliations of Benoit Dérijard include University of California, San Diego & University of Massachusetts Medical School.

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JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain

TL;DR: JNK1 is a component of a novel signal transduction pathway that is activated by oncoproteins and UV irradiation and its properties indicate that JNK1 activation may play an important role in tumor promotion.
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Independent human MAP kinase signal transduction pathways defined by MEK and MKK isoforms

TL;DR: It is demonstrated that the activators of p38, MKK3 and MKK4, JNK (MKK4), and ERK (MEK1 and MEK2) define independent MAP kinase signal transduction pathways.
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Transcription Factor ATF2 Regulation by the JNK Signal Transduction Pathway

TL;DR: A role for the JNK signal transduction pathway in transcriptional responses mediated by ATF2 is demonstrated and mutations in this pathway inhibited ATF2-stimulated gene expression mediated by the retinoblastoma tumor suppressor and the adenovirus early region 1A (E1A) oncoprotein.
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Selective interaction of JNK protein kinase isoforms with transcription factors.

TL;DR: Comparison of the binding activity of the JNK isoforms demonstrated that the J NK proteins differ in their interaction with ATF2, Elk‐1 and Jun transcription factors, suggesting that individual members of theJNK group may selectively target specific transcription factors in vivo.
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MKK3- and MKK6-regulated gene expression is mediated by the p38 mitogen-activated protein kinase signal transduction pathway.

TL;DR: Cotransfection experiments demonstrated that p38 MAP kinase activation causes increased reporter gene expression mediated by the transcription factors ATF2 and Elk-1, demonstrating that the nucleus is one target of the p38MAP kinase signal transduction pathway.