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

Increased susceptibility to isoproterenol-induced cardiac hypertrophy and impaired weight gain in mice lacking the histidine-rich calcium-binding protein.

Molecular and cellular biology - 1 Dec 2006

Jaehnig Eric J, Heidt Analeah B, Greene Stephanie B, Cornelissen Ivo, Black Brian L

Abstract excerpt

The sarcoplasmic reticulum (SR) plays a critical role in excitation-contraction coupling by regulating the cytoplasmic calcium concentration of striated muscle. The histidine-rich calcium-binding protein (HRCBP) is expressed in the junctional SR, the site of calcium release from the SR. HRCBP is expressed exclusively in muscle tissues and binds calcium with low affinity and high capacity. In addition, HRCBP...

Read the complete abstract on PubMed

Topics

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

Share to Calcium
Share to Calcium-Binding Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cardiomegaly

Share to Isoproterenol

Share to Mice, Knockout

Share to Muscle Proteins

Share to Muscle, Skeletal

Share to Weight Gain

Source

Open in PubMed Open full text

Identifiers

PMID: 17030629
DOI: 10.1128/MCB.00482-06
PMCID: PMC1698540

Genes

HRC

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

Increased susceptibility to isoproterenol-induced cardiac hypertrophy and impaired weight gain in mice lacking the histidine-rich calcium-binding protein.PMID 17030629Read ↗

Targeted ablation of the histidine-rich Ca(2+)-binding protein (HRC) gene is associated with abnormal SR Ca(2+)-cycling and severe pathology under pressure-overload stress.Semantic proximity Read ↗

AAV-mediated knock-down of HRC exacerbates transverse aorta constriction-induced heart failure.Semantic proximity Read ↗

Impaired calcium homeostasis is associated with sudden cardiac death and arrhythmias in a genetic equivalent mouse model of the human HRC-Ser96Ala variantSemantic proximity Read ↗

Phosphorylation of serine96 of histidine-rich calcium-binding protein by the Fam20C kinase functions to prevent cardiac arrhythmia.Semantic proximity Read ↗

Proteins within the intracellular calcium store determine cardiac RyR channel activity and cardiac output.Semantic proximity Read ↗

Junctophilin-2 physically interacts with ryanodine receptor type 2 for peripheral coupling of mouse cardiomyocytesSemantic 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 ↗

Defective beta-adrenergic receptor signaling precedes the development of dilated cardiomyopathy in transgenic mice with calsequestrin overexpression.Semantic proximity Read ↗

Cardiac-specific overexpression of a high Ca2+ affinity mutant of SERCA2a attenuates in vivo pressure overload cardiac hypertrophy.Semantic proximity Read ↗

Endoplasmic reticulum resident protein 44 (ERp44) deficiency in mice and zebrafish leads to cardiac developmental and functional defects.Semantic proximity Read ↗

Characterization of Ca(2+)-Dependent Protein-Protein Interactions within the Ca(2+) Release Units of Cardiac Sarcoplasmic Reticulum.Semantic proximity Read ↗

Mice lacking calsarcin-1 are sensitized to calcineurin signaling and show accelerated cardiomyopathy in response to pathological biomechanical stress.Semantic proximity Read ↗

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