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Verfasst von:Peuckert, Christiane [VerfasserIn]   i
 Aresh, Bejan [VerfasserIn]   i
 Holenya, Pavlo [VerfasserIn]   i
 Adams, Derek [VerfasserIn]   i
 Sreedharan, Smitha [VerfasserIn]   i
 Porthin, Annika [VerfasserIn]   i
 Andersson, Louise [VerfasserIn]   i
 Pettersson, Hanna [VerfasserIn]   i
 Wölfl, Stefan [VerfasserIn]   i
 Klein, Rüdiger [VerfasserIn]   i
 Oxburgh, Leif [VerfasserIn]   i
 Kullander, Klas [VerfasserIn]   i
Titel:Multimodal Eph/Ephrin signaling controls several phases of urogenital development
Verf.angabe:Christiane Peuckert, Bejan Aresh, Pavlo Holenya, Derek Adams, Smitha Sreedharan, Annika Porthin, Louise Andersson, Hanna Pettersson, Stefan Wölfl, Rüdiger Klein, Leif Oxburgh, Klas Kullander
E-Jahr:2016
Jahr:22 June 2016
Umfang:16 S.
Fussnoten:Published online 22 June 2016 ; Gesehen am 13.10.2020
Titel Quelle:Enthalten in: Kidney international
Ort Quelle:New York, NY : Elsevier, 1972
Jahr Quelle:2016
Band/Heft Quelle:90(2016), 2, Seite 373-388
ISSN Quelle:1523-1755
Abstract:A substantial portion of the human population is affected by urogenital birth defects resulting from a failure in ureter development. Although recent research suggests roles for several genes in facilitating the ureter/bladder connection, the underlying molecular mechanisms remain poorly understood. Signaling via Eph receptor tyrosine kinases is involved in several developmental processes. Here we report that impaired Eph/Ephrin signaling in genetically modified mice results in severe hydronephrosis caused by defective ureteric bud induction, ureter maturation, and translocation. Our data imply that ureter translocation requires apoptosis in the urogenital sinus and inhibition of proliferation in the common nephric duct. These processes were disturbed in EphA4/EphB2 compound knockout mice and were accompanied by decreased ERK-2 phosphorylation. Using a set of Eph, Ephrin, and signaling-deficient mutants, we found that during urogenital development, different modes of Eph/Ephrin signaling occur at several sites with EphrinB2 and EphrinA5 acting in concert. Thus, Eph/Ephrin signaling should be considered in the etiology of congenital kidney and urinary tract anomalies.
DOI:doi:10.1016/j.kint.2016.04.021
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.kint.2016.04.021
 Volltext: http://www.sciencedirect.com/science/article/pii/S0085253816301946
 DOI: https://doi.org/10.1016/j.kint.2016.04.021
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:CAKUT
 common nephric duct
 Eph
 Ephrin
 ureteric bud
 urogenital sinus
K10plus-PPN:1735485217
Verknüpfungen:→ Zeitschrift

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