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@ARTICLE{Bueno:917388,
      author       = {Bueno, Diones and Dey, Partha Narayan 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
                      Schäfer, Michael K. E. and Florin, Luise and Gomez-Zepeda,
                      David and Tenzer, Stefan 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 and Ritz, Sandra and Peper,
                      Jonas and Silies, Marion and Frauenknecht, Katrin B. M. and
                      Methner, Axel},
      title        = {{NECAB}2 participates in an endosomal pathway of
                      mitochondrial stress response at striatal synapses},
      journal      = {bioRxiv beta},
      address      = {Cold Spring Harbor},
      publisher    = {Cold Spring Harbor Laboratory, NY},
      reportid     = {FZJ-2023-00602},
      year         = {2021},
      abstract     = {Synaptic signaling depends on ATP generated by
                      mitochondria. Due to extensive connectivity, the striatum is
                      especially vulnerable to mitochondrial dysfunction and thus
                      requires efficient mitochondrial quality control and repair.
                      We found that global knockout of the neuronal
                      calcium-binding protein 2 (NECAB2) in the mouse causes loss
                      of striatal synapses and behavioral phenotypes related to
                      striatal dysfunction such as reduced motivation and altered
                      sensory gating. Striatal mitochondria from Necab2 knockout
                      mice are more abundant and smaller. They are characterized
                      by increased respiration and superoxide production resulting
                      in oxidative stress. This accumulation of dysfunctional
                      mitochondria is caused by a defective assembly of
                      mitochondria with early endosomes in a pathway that involves
                      the small GTPase Rab5 and its guanine nucleotide exchange
                      factor Alsin/ALS2. NECAB2 therefore participates in an
                      endosomal pathway of mitochondrial stress response and
                      repair important for striatal function.},
      cin          = {INM-2},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5252},
      typ          = {PUB:(DE-HGF)25},
      doi          = {10.1101/2021.02.15.431234},
      url          = {https://juser.fz-juelich.de/record/917388},
}