001     917388
005     20230123101927.0
024 7 _ |2 doi
|a 10.1101/2021.02.15.431234
024 7 _ |2 Handle
|a 2128/33587
037 _ _ |a FZJ-2023-00602
082 _ _ |a 570
100 1 _ |0 0000-0002-8064-6412
|a Bueno, Diones
|b 0
245 _ _ |a NECAB2 participates in an endosomal pathway of mitochondrial stress response at striatal synapses
260 _ _ |a Cold Spring Harbor
|b Cold Spring Harbor Laboratory, NY
|c 2021
336 7 _ |0 PUB:(DE-HGF)25
|2 PUB:(DE-HGF)
|a Preprint
|b preprint
|m preprint
|s 1673615981_4157
336 7 _ |2 ORCID
|a WORKING_PAPER
336 7 _ |0 28
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|a Electronic Article
336 7 _ |2 DRIVER
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336 7 _ |2 BibTeX
|a ARTICLE
336 7 _ |2 DataCite
|a Output Types/Working Paper
520 _ _ |a 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.
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700 1 _ |0 P:(DE-HGF)0
|a Dey, Partha Narayan
|b 1
700 1 _ |0 P:(DE-HGF)0
|a Schacht, Teresa
|b 2
700 1 _ |0 P:(DE-HGF)0
|a Wolf, Christina
|b 3
700 1 _ |0 P:(DE-HGF)0
|a Wüllner, Verena
|b 4
700 1 _ |0 0000-0002-8361-8134
|a Morpurgo, Elena
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700 1 _ |0 P:(DE-HGF)0
|a Rojas-Charry, Liliana
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|a Sessinghaus, Lena
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|a Schäfer, Michael K. E.
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|a Florin, Luise
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|a Gomez-Zepeda, David
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700 1 _ |0 0000-0003-3034-0017
|a Tenzer, Stefan
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|a Baumgart, Jan
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700 1 _ |0 P:(DE-HGF)0
|a Stamm, Paul
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700 1 _ |0 P:(DE-HGF)0
|a Daiber, Andreas
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700 1 _ |0 P:(DE-HGF)0
|a Horta, Guilherme
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700 1 _ |0 P:(DE-HGF)0
|a Nardi, Leonardo
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700 1 _ |0 P:(DE-HGF)0
|a Vasic, Verica
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700 1 _ |0 0000-0002-5514-1922
|a Schmeisser, Michael J.
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700 1 _ |0 0000-0001-7337-6007
|a Anand, Ruchika
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700 1 _ |0 P:(DE-Juel1)171721
|a Reichert, Andreas
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700 1 _ |0 P:(DE-HGF)0
|a Ritz, Sandra
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700 1 _ |0 P:(DE-HGF)0
|a Peper, Jonas
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700 1 _ |0 0000-0003-2810-9828
|a Silies, Marion
|b 29
700 1 _ |0 0000-0002-1372-3297
|a Frauenknecht, Katrin B. M.
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700 1 _ |0 0000-0002-8774-0057
|a Methner, Axel
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773 _ _ |0 PERI:(DE-600)2766415-6
|a 10.1101/2021.02.15.431234
|t bioRxiv beta
|y 2021
856 4 _ |u https://juser.fz-juelich.de/record/917388/files/2021.02.15.431234.full.pdf
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Marc 21