scispace - formally typeset
J

Jihane Basbous

Researcher at University of Montpellier

Publications -  29
Citations -  1813

Jihane Basbous is an academic researcher from University of Montpellier. The author has contributed to research in topics: DNA damage & Transcription factor. The author has an hindex of 17, co-authored 25 publications receiving 1606 citations. Previous affiliations of Jihane Basbous include Centre national de la recherche scientifique & American University of Beirut.

Papers
More filters
Journal ArticleDOI

The Complementary Strand of the Human T-Cell Leukemia Virus Type 1 RNA Genome Encodes a bZIP Transcription Factor That Down-Regulates Viral Transcription

TL;DR: It is shown here that HBZ is able to interact with the bZIP transcription factor CREB-2 (also called ATF-4), known to activate the HTLV-1 transcription by recruiting the viral trans-activator Tax on the Tax-responsive elements (TxREs), but it is demonstrated that the HBZ/CREB- 2 heterodimers are no more able to bind to the TxRE and cyclic AMP response element sites.
Journal ArticleDOI

The HBZ Factor of Human T-cell Leukemia Virus Type I Dimerizes with Transcription Factors JunB and c-Jun and Modulates Their Transcriptional Activity

TL;DR: The hypothesis that HBZ could be a negative modulator of the Tax effect by controlling Tax expression at the transcriptional level and by attenuating activation of AP-1 by Tax is supported.
Journal ArticleDOI

Premature Activation of the SLX4 Complex by Vpr Promotes G2/M Arrest and Escape from Innate Immune Sensing

TL;DR: The identity of the cellular factors required for Vpr-mediated G2/M arrest is revealed and the SLX4com is identified as a regulator of innate immunity.
Journal ArticleDOI

HBZ interacts with JunD and stimulates its transcriptional activity.

TL;DR: It is shown that HBZ can activate JunD‐dependent transcription and that its amino‐terminus is required, and that this association occurs via the bZIP domain of the two proteins.
Journal ArticleDOI

Ubiquitin-independent proteasomal degradation of Fra-1 is antagonized by Erk1/2 pathway-mediated phosphorylation of a unique C-terminal destabilizer.

TL;DR: The presence of a single destabilizer within Fra-1, instead of two that are differentially regulated in c-Fos, explains the much faster turnover of the latter when cells traverse the G0/G1-to-S-phase transition.