ArticleMolecular and cellular biology2006
Increased susceptibility to isoproterenol-induced cardiac hypertrophy and impaired weight gain in mice lacking the histidine-rich calcium-binding protein.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- An injury-responsiveScience advances · 2023Article
- Evaluation of Anti-hypertrophic Potential ofIndian journal of clinical biochemistry : IJCB · 2021Article
- Ablation of HRC alleviates cardiac arrhythmia and improves abnormal Ca handling in CASQ2 knockout mice prone to CPVT.Cardiovascular research · 2015Article
- Myocyte enhancer factor 2C function in skeletal muscle is required for normal growth and glucose metabolism in mice.Skeletal muscle · 2015Article
- NFATc1 controls skeletal muscle fiber type and is a negative regulator of MyoD activity.Cell reports · 2014Article
- Genetic ablation of ryanodine receptor 2 phosphorylation at Ser-2808 aggravates Ca(2+)-dependent cardiomyopathy by exacerbating diastolic Ca2+ release.The Journal of physiology · 2014Article
- Searching for sudden death snps in calcium handling genes.Journal of the American Heart Association · 2013Article
- 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.Basic research in cardiology · 2013Article
- Article
- Modulation of cardiac contractility by the phospholamban/SERCA2a regulatome.Circulation research · 2012Review
- AAV-mediated knock-down of HRC exacerbates transverse aorta constriction-induced heart failure.PloS one · 2012Article
- On the footsteps of Triadin and its role in skeletal muscle.World journal of biological chemistry · 2011Article
- Molecular and functional analyses of aspolin, a fish-specific protein extremely rich in aspartic acid.Marine biotechnology (New York, N.Y.) · 2011Article
- Organellar calcium buffers.Cold Spring Harbor perspectives in biology · 2011Review
- Histidine-rich calcium binding protein: the new regulator of sarcoplasmic reticulum calcium cycling.Journal of molecular and cellular cardiology · 2011Review
- Junctin and the histidine-rich Ca2+ binding protein: potential roles in heart failure and arrhythmogenesis.The Journal of physiology · 2009Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
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 interacts with triadin, a protein associated with the ryanodine receptor and thought to be involved in calcium release. Its calcium binding properties, localization to the SR, and interaction with triadin suggest that HRCBP is involved in calcium handling by the SR. To determine the function of HRCBP in vivo, we inactivated HRC, the gene encoding HRCBP, in mice. HRC knockout mice exhibited impaired weight gain beginning at 11 months of age, which was marked by reduced skeletal muscle and fat mass, and triadin protein expression was upregulated in the heart of HRC knockout mice. In addition, HRC null mice displayed a significantly exaggerated response to the induction of cardiac hypertrophy by isoproterenol compared to their wild-type littermates. The exaggerated response of HRC knockout mice to the induction of cardiac hypertrophy is consistent with a regulatory role for HRCBP in calcium handling in vivo and suggests that mutations in HRC, in combination with other genetic or environmental factors, might contribute to pathological hypertrophy and heart failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.