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

Glycogen synthase kinase-3beta is a negative regulator of cardiomyocyte hypertrophy.

The Journal of cell biology - 2 Oct 2000

Haq S, Choukroun G, Kang Z B, Ranu H, Matsui T, Rosenzweig A, Molkentin J D, Alessandrini A, Woodgett J, Hajjar R, Michael A, Force T

Abstract excerpt

Hypertrophy is a basic cellular response to a variety of stressors and growth factors, and has been best characterized in myocytes. Pathologic hypertrophy of cardiac myocytes leads to heart failure, a major cause of death and disability in the developed world. Several cytosolic signaling pathways have been identified that transduce prohypertrophic signals, but to date, little work has focused on signaling...

Read the complete abstract on PubMed

Topics

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

Share to Phenylephrine
Share to Animals, Newborn

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Calcium-Calmodulin-Dependent Protein Kinases

Share to Cardiomegaly

Share to Endothelin-1

Share to Glycogen Synthase Kinase 3

Share to Myocardium

Share to NFATC Transcription Factors

Source

Open in PubMed Open full text

Identifiers

PMID: 11018058
DOI: 10.1083/jcb.151.1.117
PMCID: PMC2189812

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Glycogen synthase kinase-3beta is a negative regulator of cardiomyocyte hypertrophy.PMID 11018058Read ↗

Unique and overlapping functions of GSK-3 isoforms in cell differentiation and proliferation and cardiovascular development.Semantic proximity Read ↗

Interferon regulatory factor 3 is a negative regulator of pathological cardiac hypertrophySemantic proximity Read ↗

Constitutive glycogen synthase kinase-3alpha/beta activity protects against chronic beta-adrenergic remodelling of the heart.Semantic proximity Read ↗

Cardiac fibroblast GSK-3α mediates adverse myocardial fibrosis via IL-11 and ERK pathwaySemantic proximity Read ↗

The role of Akt/GSK-3beta signaling in familial hypertrophic cardiomyopathy.Semantic proximity Read ↗

Blocking cardiac growth in hypertrophic cardiomyopathy induces cardiac dysfunction and decreased survival only in males.Semantic proximity Read ↗

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

Deletion of Cardiomyocyte Glycogen Synthase Kinase-3 Beta (GSK-3β) Improves Systemic Glucose Tolerance with Maintained Heart Function in Established Obesity.Semantic proximity Read ↗

Glycogen synthase kinase 3beta is a negative regulator of growth factor-induced activation of the c-Jun N-terminal kinase.Semantic proximity Read ↗

Anchored p90 ribosomal S6 kinase 3 is required for cardiac myocyte hypertrophy.Semantic proximity Read ↗

Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH(2)-terminal kinases.Semantic proximity Read ↗

GSK-3α is a central regulator of age-related pathologies in mice.Semantic proximity Read ↗

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