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MYBPC3 encodes the cardiac isoform of myosin-binding protein C. Additionally we are shipping MYBPC3 Kits (14) and MYBPC3 Proteins (4) and many more products for this protein.
Showing 10 out of 64 products:
Human Polyclonal MYBPC3 Primary Antibody for EIA, IHC (p) - ABIN953556
Bailey, Xie, Do, Montpetit, Diaz, Mohan, Keavney, Yusuf, Gerstein, Engert, Anand: Variation at the NFATC2 locus increases the risk of thiazolidinedione-induced edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) study. in Diabetes Care 2010
Show all 5 references for ABIN953556
N terminus of cMyBP-C interacts with F-actin through multiple distinct binding sites and that binding at one or more sites is reduced by phosphorylation
Crypts are a normal part of cardiac development but, along with the mitral valve and trabeculae, their developmental trajectory is altered by the presence of HCM truncating Mybpc3 gene mutation
that in the homozygous hypertrophic cardiomyopathy mouse model, beta-AR stimulation leads to preferential PKA phosphorylation of phospholamban over cardiac troponin I, resulting in an impaired inotropic and lusitropic response
Phosphorylation of MYBPC3 contributes to the genesis of ventricular wall geometry, linking myofilament biology with multiscale cardiac mechanics and myoarchitecture.
The cMyBP-C hypertrophic cardiomyopathy variant L348P enhances thin filament activation through an increased shift in tropomyosin (show TPM2 Antibodies) position.
The contributions of cardiac myosin binding protein C and troponin I phosphorylation to beta-adrenergic enhancement of in vivo cardiac function
MYBPC3 mutations is elevated oxidative stress that corresponded to severe cardiac dysfunction, myocyte damage, and myocardial remodeling.
MBPC and troponin-I phosphorylation modulate myofilament length-dependent activation
MYBPC has unexpected inhibitory functions during postnatal myocyte cytokinesis and cell cycle progression.
Haploinsufficiency occurs in heterozygote MYBPC3 mutant carriers.
cMyBP-C is a principal mediator of increased contractility observed with beta-adrenergic stimulation or increased pacing because of protein kinase A and CaMKIIdelta phosphorylations of cMyB (show MYB Antibodies)-C.
we report a patient presenting with a complex phenotype consisting of severe, adult-onset, dilated cardiomyopathy, hearing loss and developmental delay, in which exome sequencing revealed two genetic variants that are inherited from a healthy mother: a variant, in MYBPC3, that is associated with hereditary cardiomyopathy.
5 out of 102 (4.9%) athletes carried mutations: a heterozygous MYH7 (show MYH7 Antibodies) Glu935Lys mutation, a heterozygous MYBPC3 Arg160Trp mutation and another heterozygous MYBPC3 Thr1046Met mutation, all of which had been reported as HCM-associated mutations
a significant role of MYBPC3 gene mutations in Hypertrophic cardiomyopathy(HCM) disease and can be used for pre-symptomatic diagnosis of at risk family members of affected individuals.
Atrial fibrillation occurred in 74 patients with hypertrophic cardiomyopathy (31%), but with no difference among genotype groups (31% in MYBPC3, 37% in MYH7 (show MYH7 Antibodies) and 18% in other genotypes, p = 0.15).
The detection of MYBPC3 mutation, especially the PTC (show F9 Antibodies) mutation and double-mutation, may serve as a molecular marker for clinical risk stratification of HCM.
Demonstrate that MYBPC3 gene mutations, revealed by next-generation sequencing, were associated with familial and sporadic restrictive cardiomyopathy phenotype in patients.
Data indicate that homozygous or compound heterozygous truncating pathogenic myosin binding (show PPP1R12A Antibodies) protein C (show PROC Antibodies) (MYBPC3) mutations cause severe neonatal cardiomyopathy with features of left ventricular noncompaction and septal defects.
Mutations in the MYBPC3 and CASQ2 (show CASQ2 Antibodies) genes and six combinations between loci in the MYBPC3, MYH7 (show MYH7 Antibodies) and CASQ2 (show CASQ2 Antibodies) genes were responsible for cardiomyopathy risk in a studied cohort.
Although females with MYBPC3 mutations showed later onset of hypertrophic cardiomyopathy, female patients were more symptomatic at diagnosis and had more frequent heart failure events once they had developed hypertrophy.
A founder MYBPC3 mutation results in HCM with a high risk of sudden death after the fourth decade of life
small es, CyrillicMyBP-C modulates interaction of myosin with actin
MYBPC3 encodes the cardiac isoform of myosin-binding protein C. Myosin-binding protein C is a myosin-associated protein found in the cross-bridge-bearing zone (C region) of A bands in striated muscle. MYBPC3, the cardiac isoform, is expressed exclussively in heart muscle. Regulatory phosphorylation of the cardiac isoform in vivo by cAMP-dependent protein kinase (PKA) upon adrenergic stimulation may be linked to modulation of cardiac contraction. Mutations in MYBPC3 are one cause of familial hypertrophic cardiomyopathy.
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