Key result
CK2-mediated phosphorylation of angiotensin-converting enzyme (ACE) regulates its retention in the endothelial cell plasma membrane and decreases its shedding.
Why the study?
Does CK2-mediated phosphorylation of ACE regulate its retention in the endothelial cell plasma membrane?
Population
Endothelial cells (wild-type, ACE-overexpressing, and mutant ACEDeltaS-overexpressing)
Comparison
CK2 inhibition or mutation of ACE cytoplasmic… vs Untreated endothelial cells or wild-type…
Design
Preclinical
Authors
Loading...
Provides mechanistic insight in animals; leaves open whether CK2 targeting alters soluble ACE or outcomes in humans.
Does CK2-mediated phosphorylation of ACE regulate its retention in the endothelial cell plasma membrane?
CK2-mediated phosphorylation of the ACE cytoplasmic tail regulates its retention in the endothelial plasma membrane, providing a mechanism for the determination of soluble plasma ACE levels.
Kohlstedt et al. (2002) studied this question. CK2-mediated phosphorylation was evaluated on ACE phosphorylation and secretion/shedding. CK2-mediated phosphorylation of angiotensin-converting enzyme (ACE) regulates its retention in the endothelial cell plasma membrane and decreases its shedding.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: