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Verfasst von:Leibfried, Andrea [VerfasserIn]   i
 Fricke, Robert Patrick [VerfasserIn]   i
 Morgan, Matthew J. [VerfasserIn]   i
 Bogdan, Sven [VerfasserIn]   i
 Bellaïche, Yohanns [VerfasserIn]   i
Titel:Drosophila Cip4 and WASp define a branch of the Cdc42-Par6-aPKC pathway regulating E-Cadherin endocytosis
Verf.angabe:Andrea Leibfried, Robert Fricke, Matthew J. Morgan, Sven Bogdan, and Yohanns Bellaiche
E-Jahr:2008
Jahr:November 2008
Umfang:10 S.
Fussnoten:Gesehen am 08.05.2023
Titel Quelle:Enthalten in: Current biology
Ort Quelle:London : Current Biology Ltd., 1991
Jahr Quelle:2008
Band/Heft Quelle:18(2008), 21 vom: Nov., Seite 1639-1648
ISSN Quelle:1879-0445
Abstract:Background - Integral to the function and morphology of the epithelium is the lattice of cell-cell junctions known as adherens junctions (AJs). AJ stability and plasticity relies on E-Cadherin exocytosis and endocytosis. A mechanism regulating E-Cadherin (E-Cad) exocytosis to the AJs has implicated proteins of the exocyst complex, but mechanisms regulating E-Cad endocytosis from the AJs remain less well understood. - Results - Here we show that Cdc42, Par6, or aPKC loss of function is accompanied by the accumulation of apical E-Cad intracellular punctate structures and the disruption of AJs in Drosophila epithelial cells. These punctate structures derive from large and malformed endocytic vesicles that emanate from the AJs; a phenotype that is also observed upon blocking vesicle scission in dynamin mutant cells. We demonstrate that the Drosophila Cdc42-interacting protein 4 (Cip4) is a Cdc42 effector that interacts with Dynamin and the Arp2/3 activator WASp in Drosophila. Accordingly, Cip4, WASp, or Arp2/3 loss of function also results in defective E-Cadherin endocytosis. - Conclusion - Altogether our results show that Cdc42 functions with Par6 and aPKC to regulate E-Cad endocytosis and define Cip4 and WASp as regulators of the early E-Cad endocytic events in epithelial tissue.
DOI:doi:10.1016/j.cub.2008.09.063
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1016/j.cub.2008.09.063
 Volltext: https://www.sciencedirect.com/science/article/pii/S0960982208013419
 DOI: https://doi.org/10.1016/j.cub.2008.09.063
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:CELLBIO
 DEVBIO
K10plus-PPN:1844751155
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