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Schmidt, M.V.* ; Schülke, .J.-P.* ; Liebl, C.* ; Stiess, M.* ; Avrabos, C.* ; Bock, J.* ; Wochnik, GM.* ; Davies, H.A.* ; Zimmermann, N.* ; Scharf, S.H.* ; Trümbach, D. ; Wurst, W. ; Zieglgänsberger, W.* ; Turck, C.* ; Holsboer, F.* ; Stewart, M.G.* ; Bradke, F.* ; Eder, M.* ; Müller, M.B.* ; Rein, T.

Tumor suppressor down-regulated in renal cell carcinoma 1 (DRR1) is a stress-induced actin bundling factor that modulates synaptic efficacy and cognition.

Proc. Natl. Acad. Sci. U.S.A. 108, 17213-17218 (2011)
Verlagsversion DOI
Free by publisher
Stress has been identified as a major causal factor for many mental disorders. However, our knowledge about the chain of molecular and cellular events translating stress experience into altered behavior is still rather scant. Here, we have characterized a murine ortholog of the putative tumor suppressor gene DRR1 as a unique stress-induced protein in brain. It binds to actin, promotes bundling and stabilization of actin filaments, and impacts on actin-dependent neurite outgrowth. Endogenous DRR1 localizes to some, but not all, synapses, with preference for the presynaptic region. Hippocampal virus-mediated enhancement of DRR1 expression reduced spine density, diminished the probability of synaptic glutamate release, and altered cognitive performance. DRR1 emerges as a protein to link stress with actin dynamics, which in addition is able to act on synaptic function and cognition.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter actin dynamics; stress physiology; stress regulation; synaptic plasticity; TU3A
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Quellenangaben Band: 108, Heft: 41, Seiten: 17213-17218 Artikelnummer: , Supplement: ,
Verlag National Academy of Sciences
Verlagsort Washington, DC, USA
Begutachtungsstatus Peer reviewed