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@ARTICLE{Bueno:1015426,
author = {Bueno, Diones and Narayan Dey, Partha and Schacht, Teresa
and Wolf, Christina and Wüllner, Verena and Morpurgo, Elena
and Rojas-Charry, Liliana and Sessinghaus, Lena and Leukel,
Petra and Sommer, Clemens and Radyushkin, Konstantin and
Florin, Luise and Baumgart, Jan and Stamm, Paul and Daiber,
Andreas and Horta, Guilherme and Nardi, Leonardo and Vasic,
Verica and Schmeisser, Michael J. and Hellwig, Andrea and
Oskamp, Angela and Bauer, Andreas and Anand, Ruchika and
Reichert, Andreas S. and Ritz, Sandra and Nocera, Gianluigi
and Jacob, Claire and Peper, Jonas and Silies, Marion and
Frauenknecht, Katrin B. M. and Schäfer, Michael K. E. and
Methner, Axel},
title = {{NECAB}2 is an endosomal protein important for striatal
function},
journal = {Free radical biology and medicine},
volume = {208},
issn = {0891-5849},
address = {New York, NY [u.a.]},
publisher = {Elsevier},
reportid = {FZJ-2023-03683},
pages = {643 - 656},
year = {2023},
note = {Postprint liegt mir aktuell leider nicht vor},
abstract = {Synaptic signaling depends on ATP generated by
mitochondria. Dysfunctional mitochondria shift the redox
balance towards a more oxidative environment. Due to
extensive connectivity, the striatum is especially
vulnerable to mitochondrial dysfunction. We found that
neuronal calcium-binding protein 2 (NECAB2) plays a role in
striatal function and mitochondrial homeostasis. NECAB2 is a
predominantly endosomal striatal protein which partially
colocalizes with mitochondria. This colocalization is
enhanced by mild oxidative stress. Global knockout of Necab2
in the mouse results in increased superoxide levels,
increased DNA oxidation and reduced levels of the
antioxidant glutathione which correlates with an altered
mitochondrial shape and function. Striatal mitochondria from
Necab2 knockout mice are more abundant and smaller and
characterized by a reduced spare capacity suggestive of
intrinsic uncoupling respectively mitochondrial dysfunction.
In line with this, we also found an altered stress-induced
interaction of endosomes with mitochondria in Necab2
knockout striatal cultures. The predominance of
dysfunctional mitochondria and the pro-oxidative redox
milieu correlates with a loss of striatal synapses and
behavioral changes characteristic of striatal dysfunction
like reduced motivation and altered sensory gating. Together
this suggests an involvement of NECAB2 in an endosomal
pathway of mitochondrial stress response important for
striatal function.},
cin = {INM-2},
ddc = {610},
cid = {I:(DE-Juel1)INM-2-20090406},
pnm = {5253 - Neuroimaging (POF4-525) / 5252 - Brain Dysfunction
and Plasticity (POF4-525)},
pid = {G:(DE-HGF)POF4-5253 / G:(DE-HGF)POF4-5252},
typ = {PUB:(DE-HGF)16},
pubmed = {37722569},
UT = {WOS:001083542200001},
doi = {10.1016/j.freeradbiomed.2023.09.003},
url = {https://juser.fz-juelich.de/record/1015426},
}