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Mutant Cullin causes cardiovascular compromise

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Item Type:Editorial
Title:Mutant Cullin causes cardiovascular compromise
Creators Name:Luft, F.C.
Abstract:Mendelian hypertension is rare; however, Mendelian syndromes have taught us an amazing amount about mechanisms of distal sodium and chloride reabsorption, as well as how systemic hypertension might come about. In this issue of EMBO Molecular Medicine, Schumacher et al (2015) present a mouse model of the Cullin‐3 (CUL3Δ403–459) mutation, which causes a form of pseudohypoaldosteronism type‐2 (PHA‐2). CUL3 is involved in ubiquitination. Surprising is the severity of the hypertension, which may be explained in part on the basis of CUL3 actions in vascular cells. The findings underscore the role of "cleanup" in the maintenance of normal physiology.
Keywords:Animal Disease Models, Cullin Proteins, Mutation, Pseudohypoaldosteronism, Animals
Source:EMBO Molecular Medicine
ISSN:1757-4676
Publisher:Wiley-Blackwell
Volume:7
Number:10
Page Range:1254-1256
Date:1 October 2015
Official Publication:https://doi.org/10.15252/emmm.201505620
PubMed:View item in PubMed

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