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Artikel ; Online: Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry.

Bock, Fabian / Dong, Xinyu / Li, Shensen / Viquez, Olga M / Sha, Eric / Tantengco, Matthew / Hennen, Elizabeth M / Plosa, Erin / Ramezani, Alireza / Brown, Kyle L / Whang, Young Mi / Terker, Andrew S / Arroyo, Juan Pablo / Harrison, David G / Fogo, Agnes / Brakebusch, Cord H / Pozzi, Ambra / Zent, Roy

Science advances

2024  Band 10, Heft 6, Seite(n) eadi7840

Abstract: Prolonged obstruction of the ureter, which leads to injury of the kidney collecting ducts, results in permanent structural damage, while early reversal allows for repair. Cell structure is defined by the actin cytoskeleton, which is dynamically organized ...

Abstract Prolonged obstruction of the ureter, which leads to injury of the kidney collecting ducts, results in permanent structural damage, while early reversal allows for repair. Cell structure is defined by the actin cytoskeleton, which is dynamically organized by small Rho guanosine triphosphatases (GTPases). In this study, we identified the Rho GTPase, Rac1, as a driver of postobstructive kidney collecting duct repair. After the relief of ureteric obstruction, Rac1 promoted actin cytoskeletal reconstitution, which was required to maintain normal mitotic morphology allowing for successful cell division. Mechanistically, Rac1 restricted excessive actomyosin activity that stabilized the negative mitotic entry kinase Wee1. This mechanism ensured mechanical G
Mesh-Begriff(e) Kidney Tubules, Collecting/metabolism ; rac1 GTP-Binding Protein/metabolism ; Cytoskeleton/metabolism ; Actins/metabolism ; Actin Cytoskeleton/metabolism
Chemische Substanzen rac1 GTP-Binding Protein (EC 3.6.5.2) ; Actins
Sprache Englisch
Erscheinungsdatum 2024-02-07
Erscheinungsland United States
Dokumenttyp Journal Article
ZDB-ID 2810933-8
ISSN 2375-2548 ; 2375-2548
ISSN (online) 2375-2548
ISSN 2375-2548
DOI 10.1126/sciadv.adi7840
Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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