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June 20, 2000Proceedings of the National Academy of SciencesOpen Access

G protein-coupled receptor kinase-5 regulates thrombin-activated signaling in endothelial cells

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Population

Endothelial cells

Comparison

Expression of wild-type and dominant negative… vs Other GRK isoforms (GRK2, GRK6) or control

Design

Preclinical

Authors

CTChinnaswamy TiruppathìWYWeihong YanRSRaudel Sandoval

Discussion

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Overview

Identifies GRK5 as regulator of endothelial barrier in thrombin signaling; leaves open therapeutic translation from animal models.

Structured PICO

P
Population
Endothelial cells
I
Intervention
Expression of wild-type and dominant negative (dn) mutants of GRK isoforms (GRK2, GRK5, GRK6), specifically GRK5 overexpression
C
Comparator
Other GRK isoforms (GRK2, GRK6) or control
O
Outcome
Thrombin-activated signaling responses (phosphoinositide hydrolysis, intracellular Ca2+ concentration, transendothelial monolayer electrical resistance, PAR-1 phosphorylation)surrogate

GRK5 plays a crucial role in the mechanism of thrombin-induced desensitization of PAR-1 in endothelial cells, regulating endothelial barrier function.

Cite This Study

Tiruppathì et al. (2000) studied this question.

synapsesocial.com/papers/6a6fbee72163a0a01bc403eehttps://doi.org/10.1073/pnas.97.13.7440
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Also Consider

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  5. 5Mechanistic insights into how g protein-coupled receptor kinases (GRKs) regulate thrombopoiesis2025