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Edurne Berra

Researcher at Centre national de la recherche scientifique

Publications -  35
Citations -  7367

Edurne Berra is an academic researcher from Centre national de la recherche scientifique. The author has contributed to research in topics: Transcription factor & Angiogenesis. The author has an hindex of 27, co-authored 33 publications receiving 7008 citations. Previous affiliations of Edurne Berra include Cooperative Research Centre & University of Nice Sophia Antipolis.

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HIF prolyl‐hydroxylase 2 is the key oxygen sensor setting low steady‐state levels of HIF‐1α in normoxia

TL;DR: It is shown that specific ‘silencing’ of PHD2 with short interfering RNAs is sufficient to stabilize and activate HIF‐1α in normoxia in all the human cells investigated, concluding that, in vivo, PHDs have distinct assigned functions.
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p42/p44 mitogen-activated protein kinases phosphorylate hypoxia-inducible factor 1alpha (HIF-1alpha) and enhance the transcriptional activity of HIF-1.

TL;DR: It is reported here that HIF-1α is strongly phosphorylated in vivo and that phosphorylation is responsible for the marked differences in the migration pattern of Hif-1 α, and that activation of the p42/p44 MAPK pathway in quiescent cells induced theosphorylation and shift of HIF -1α.
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Prolyl hydroxylase-1 negatively regulates IκB kinase-β, giving insight into hypoxia-induced NFκB activity

TL;DR: It is hypothesized that hypoxia releases repression of NFκB activity through decreased PHD-dependent hydroxylation of IKKβ, an event that may contribute to tumor development and progression through amplification of tumorigenic signaling pathways.
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Nonhypoxic Pathway Mediates the Induction of Hypoxia-inducible Factor 1α in Vascular Smooth Muscle Cells *

TL;DR: It is reported here that HIF-1alpha protein levels are strongly increased by fetal calf serum in quiescent VSMC, and strong induction of VEGF mRNA by Ang II can also be inhibited by these ROS inhibitors.
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JunD Reduces Tumor Angiogenesis by Protecting Cells from Oxidative Stress

TL;DR: JunD, a member of the AP-1 family of transcription factors, reduces tumor angiogenesis by limiting Ras-mediated production of ROS and provides new insights into the regulation of PHD activity, allowing immediate reactive adaptation to changes in O2 or iron levels in the cell.