Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Gα(i2)-mediated protection from ischaemic injury is modulated by endogenous RGS proteins in the mouse heart.

Cardiovascular research - 1 Jul 2011

Waterson Rachael E, Thompson Corbin G, Mabe Nathaniel W, Kaur Kuljeet, Talbot Jeffery N, Neubig Richard R, Rorabaugh Boyd R

Abstract excerpt

AIMS: Regulator of G protein signalling (RGS) proteins act as molecular 'off switches' that terminate G protein signalling by catalyzing the hydrolysis of Gα-bound GTP to GDP. Many different Gα(i)-coupled receptors have been implicated in the cardioprotective effects of ischaemic preconditioning. However, the role of RGS proteins in modulating cardioprotection has not been previously investigated. We used mice...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cardiotonic Agents
Share to KATP Channels

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Least-Squares Analysis

Share to Myocardial Contraction

Share to Myocardial Reperfusion Injury

Share to Perfusion

Share to Potassium Channel Blockers

Share to RGS Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 21349876
DOI: 10.1093/cvr/cvr054
PMCID: PMC3112020

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Gα(i2)-mediated protection from ischaemic injury is modulated by endogenous RGS proteins in the mouse heart.PMID 21349876Read ↗

Conditional disruption of interactions between Gαi2 and regulator of G protein signaling (RGS) proteins protects the heart from ischemic injury.Semantic proximity Read ↗

RGS-Insensitive G Proteins as In Vivo Probes of RGS Function.Semantic proximity Read ↗

RGS-insensitive Gα subunits: probes of Gα subtype-selective signaling and physiological functions of RGS proteins.Semantic proximity Read ↗

Pleiotropic phenotype of a genomic knock-in of an RGS-insensitive G184S Gnai2 allele.Semantic proximity Read ↗

Deregulation of RGS2 in cardiovascular diseasesSemantic proximity Read ↗

RGS/Gi2alpha interactions modulate platelet accumulation and thrombus formation at sites of vascular injury.Semantic proximity Read ↗

Keeping the Balance Right: Regulator of G Protein Signaling 5 in Vascular Physiology and Pathology.Semantic proximity Read ↗

Expression of RGS3, RGS4 and Gi alpha 2 in acutely failing donor hearts and end-stage heart failureSemantic proximity Read ↗

Absence of the Regulator of G-protein Signaling, RGS4, Predisposes to Atrial Fibrillation and Is Associated with Abnormal Calcium Handling.Semantic proximity Read ↗

Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice.Semantic proximity Read ↗

Reduced expression of regulator of G-protein signaling 2 (RGS2) in hypertensive patients increases calcium mobilization and ERK1/2 phosphorylation induced by angiotensin II.Semantic proximity Read ↗

β-arrestin 2 mediates cardiac ischemia-reperfusion injury via inhibiting GPCR-independent cell survival signalling.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.