Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location Vocabulary mapping
Gene Ontology annotation based on curation of immunofluorescence data
Interaction of HRC (histidine-rich Ca(2+)-binding protein) and triadin in the lumen of sarcoplasmic reticulum.
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HRC resides in the SR lumen
"While HRC resides in the lumen of the sarcoplasmic reticulum, the physiological function of HRC is largely unknown"
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HRC binds directly to triadin via histidine-rich acidic repeats
"we have performed co-immunoprecipitation experiments and show that HRC binds directly to triadin"
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HRC-triadin interaction is Ca2+-dependent
"the interaction of HRC and triadin is Ca(2+)-sensitive"
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HRC may regulate Ca2+ release by interaction with triadin
"Our data suggest that HRC may play a role in the regulation of Ca(2+) release from the sarcoplasmic reticulum by interaction with triadin"
Histidine-rich Ca-binding protein interacts with sarcoplasmic reticulum Ca-ATPase.
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HRC binds directly to SERCA2a (residues 320-460 of HRC to residues 74-90 of SERCA2)
"This interaction involves the histidine- and glutamic acid-rich domain of HRC (320-460 aa) and the part of the NH(2)-terminal cation transporter domain of SERCA2 (74-90 aa) that projects into the SR lumen"
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Increased Ca2+ reduces HRC-SERCA2a binding but increases HRC-triadin binding
"increases in Ca concentration were associated with a significant reduction of HRC binding to SERCA2, whereas they had opposite effects on the HRC-triadin interaction"
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HRC overexpression decreases SR Ca uptake and delays relaxation
"HRC overexpression in transgenic mouse hearts was associated with decreased rates of SR Ca uptake and delayed relaxation"
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HRC mediates cross-talk between SR Ca uptake and release
"HRC may play a key role in the regulation of SR Ca cycling through its direct interactions with SERCA2 and triadin, mediating a fine cross talk between SR Ca uptake and release in the heart"
A novel dominant mutation in plakoglobin causes arrhythmogenic right ventricular cardiomyopathy.
The Ser96Ala variant in histidine-rich calcium-binding protein is associated with life-threatening ventricular arrhythmias in idiopathic dilated cardiomyopathy.
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Ser96Ala variant associated with ventricular arrhythmias in DCM
"the Ser96Ala polymorphism exhibited a statistically significant correlation with the occurrence of life-threatening ventricular arrhythmias"
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HR 9.620 for Ala/Ala vs Ser/Ser for ventricular arrhythmias
"the risk for ventricular arrhythmias was higher (HR, 9.620; 95% CI, 2.183-42.394; P = 0.003) in the Ala/Ala patients, compared with Ser/Ser homozygous patients"
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Ser96Ala is an independent predictor of arrhythmogenesis in DCM
"the Ser96Ala polymorphism was the only significant genetic arrythmogenesis predictor in DCM patients"
cDNA and genomic cloning of HRC, a human sarcoplasmic reticulum protein, and localization of the gene to human chromosome 19 and mouse chromosome 7.
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HRC is a 165 kDa SR luminal protein
"Histidine-rich calcium binding protein (HRC) is a luminal sarcoplasmic reticulum (SR) protein of 165 kDa"
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Contains histidine-rich calcium binding domains
"Histidine-rich calcium binding protein (HRC)"
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Gene located on chromosome 19
"the gene encoding human HRC was localized to human chromosome 19 and mouse chromosome 7"
Abnormal calcium cycling and cardiac arrhythmias associated with the human Ser96Ala genetic variant of histidine-rich calcium-binding protein.
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Ala96 HRC decreases cardiomyocyte contractility and Ca2+ kinetics
"Ala96 HRC decreased (25% to 30%) cardiomyocyte contractility and Ca2+ kinetics compared with Ser96 HRC"
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Ala96 HRC shows diminished interaction with triadin
"The underlying mechanisms involved diminished interaction of Ala96 HRC with triadin, affecting ryanodine receptor (RyR) stability"
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Increased RyR2 open probability in Ala96 HRC
"the open probability of RyR, assessed by use of ryanodine binding, was significantly increased"
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Increased Ca2+ sparks and waves leading to arrhythmias
"the frequency of Ca2+ waves was significantly higher (10-fold), although SR Ca2+ load was reduced (by 27%) in Ala96 HRC cells"
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Ala96 HRC shows increased propensity to ventricular arrhythmias
"Parallel in vivo studies revealed ventricular ectopy on short-term isoproterenol challenge and increased (4-fold) propensity to arrhythmias"
The arrhythmogenic human HRC point mutation S96A leads to spontaneous Ca(2+) release due to an impaired ability to buffer store Ca(2+).
A reference map of the human binary protein interactome.
FAM20C phosphorylates FAM20C substrates
Deep research report on HRC
Cyberian deep research on HRC function