@misc{10481/110907,
year = {2020},
month = {11},
url = {https://hdl.handle.net/10481/110907},
abstract = {Parp3 is a member of the Poly(ADP-ribose) polymerase (Parp) family that has been characterized for its functions in
strand break repair, chromosomal rearrangements, mitotic segregation and tumor aggressiveness. Yet its physiological
implications remain unknown. Here we report a central function of Parp3 in the regulation of redox homeostasis in
continuous neurogenesis in mice. We show that the absence of Parp3 provokes Nox4-induced oxidative stress and
defective mTorc2 activation leading to inefficient differentiation of post-natal neural stem/progenitor cells to
astrocytes. The accumulation of ROS contributes to the decreased activity of mTorc2 as a result of an oxidationinduced
and Fbxw7-mediated ubiquitination and degradation of Rictor. In vivo, mTorc2 signaling is compromised in
the striatum of naïve post-natal Parp3-deficient mice and 6 h after acute hypoxia-ischemia. These findings reveal a
physiological function of Parp3 in the tight regulation of striatal oxidative stress and mTorc2 during astrocytic
differentiation and in the acute phase of hypoxia-ischemia.},
organization = {USIAS-2017-029},
organization = {Ramon Areces Foundation},
organization = {Strasbourg University},
organization = {Centre National de la recherche Scientifique},
organization = {LABEX ANR-10- LABX-0034_Medalis},
organization = {“France Génomique” consortium (ANR-10-INSB-0009)},
publisher = {Springer Nature},
keywords = {PARP3},
keywords = {Neurogenesis},
keywords = {Astrocytes Differentiation},
title = {Parp3 promotes astrocytic differentiation through a tight regulation of Nox4-induced ROS and mTorc2 activation},
doi = {10.1038/s41419-020-03167-5},
author = {Rodríguez Vargas, José Manuel and Martin-Hernandez, Kathline and Wang, Wei and Kunath, Nicolas and Suganthan, Rajikala and Amé, Jean-Christophe and Oliver, F Javier and Ye, Jing and Bjørås, Magnar and Dantzer, Francoise},
}