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

The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.

Circulation research - 3 Sept 2010

Nakayama Hiroyuki, Bodi Ilona, Maillet Marjorie, DeSantiago Jaime, Domeier Timothy L, Mikoshiba Katsuhiko, Lorenz John N, Blatter Lothar A, Bers Donald M, Molkentin Jeffery D

Abstract excerpt

RATIONALE: Inositol 1,4,5-trisphosphate (IP(3)) is a second messenger that regulates intracellular Ca(2+) release through IP(3) receptors located in the sarco(endo)plasmic reticulum of cardiac myocytes. Many prohypertrophic G protein-coupled receptor (GPCR) signaling events lead to IP(3) liberation, although its importance in transducing the hypertrophic response has not been established in vivo. OBJECTIVE: Here,...

Read the complete abstract on PubMed

Topics

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

Share to Calcineurin
Share to Cardiomegaly

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Endothelin-1

Share to GTP-Binding Protein alpha Subunits, Gq-G11

Share to Inositol 1,4,5-Trisphosphate

Share to Inositol 1,4,5-Trisphosphate Receptors

Share to Isoproterenol

Share to Physical Exertion

Source

Open in PubMed Open full text

Identifiers

PMID: 20616315
DOI: 10.1161/CIRCRESAHA.110.220038
PMCID: PMC2933281

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

The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.PMID 20616315Read ↗

Functionally redundant control of cardiac hypertrophic signaling by inositol 1,4,5-trisphosphate receptorsSemantic proximity Read ↗

No contribution of IP3-R(2) to disease phenotype in models of dilated cardiomyopathy or pressure overload hypertrophy.Semantic proximity Read ↗

Inositol 1,4,5-trisphosphate-mediated sarcoplasmic reticulum-mitochondrial crosstalk influences adenosine triphosphate production via mitochondrial Ca2+ uptake through the mitochondrial ryanodine receptor in cardiac myocytes.Semantic proximity Read ↗

Phosphoinositide 3-kinase(p110alpha) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy.Semantic proximity Read ↗

Loss of receptor activity-modifying protein 3 exacerbates cardiac hypertrophy and transition to heart failure in a sex-dependent manner.Semantic proximity Read ↗

Calcium cycling proteins in heart failure, cardiomyopathy and arrhythmias.Semantic proximity Read ↗

Pathophysiological consequences of isoform-specific IP3 receptor mutations.Semantic proximity Read ↗

Cardiac-specific overexpression of AT1 receptor mutant lacking G alpha q/G alpha i coupling causes hypertrophy and bradycardia in transgenic mice.Semantic proximity Read ↗

Temporally controlled overexpression of cardiac-specific PI3Kalpha induces enhanced myocardial contractility--a new transgenic model.Semantic proximity Read ↗

Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.Semantic proximity Read ↗

Selective changes in cytosolic β-adrenergic cAMP signals and L-type Calcium Channel regulation by Phosphodiesterases during cardiac hypertrophy.Semantic proximity Read ↗

The phosphatidylinositol(4,5)bisphosphate-binding sequence of transient receptor potential channel canonical 4α is critical for its contribution to cardiomyocyte hypertrophy.Semantic proximity Read ↗

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