Myosin Binding Protein C, Cardiac (MYBPC3) ELISA Kits

Cow (Bovine) Myosin Binding Protein C, Cardiac (MYBPC3) Interaktionspartner

1. 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

Mouse (Murine) Myosin Binding Protein C, Cardiac (MYBPC3) Interaktionspartner

1. these findings suggest the possibility that Fhod3 contributes to the pathogenesis of cMyBP-C-related cardiomyopathy and that Fhod3 is critically involved in cMyBP-C-mediated regulation of cardiac function via direct interaction.

2. Diltiazem recently showed promising beneficial effects in pre-clinical HCM, particularly in patients carrying MYBPC3 mutations.

3. autophagy is impaired in Mybpc3-targeted knockin mice

4. these data indicate a robust proinflammatory response in DCM hearts, likely in response to cellular damage triggered by MYBPC3 mutation and resultant contractile dysfunction.

5. We provide evidence that haploinsufficiency and poison polypeptide hypotheses are disease mechanisms and that EHTs can be used as a platform to evaluate the direct impact of (newly identified) MYBPC3 gene variants.

6. These results support the proposal that cMyBP-C stabilises the thick filament and that the loss of cMyBP-C results in an untethering of myosin heads.

7. 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

8. 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

9. Phosphorylation of MYBPC3 contributes to the genesis of ventricular wall geometry, linking myofilament biology with multiscale cardiac mechanics and myoarchitecture.

10. The cMyBP-C hypertrophic cardiomyopathy variant L348P enhances thin filament activation through an increased shift in tropomyosin (zeige TPM2 ELISA Kits) position.

Human Myosin Binding Protein C, Cardiac (MYBPC3) Interaktionspartner

1. MYBPC3 does not seem to play a role in anthracycline induced cardiotoxicity.

2. Mutation in MYBPC3 was identified as Restrictive Cardiomyopathy - causing mutation.

3. pathogenic gene mutations in LMNA (zeige LMNA ELISA Kits) and MYBPC3 alter RNA splicing and may have a role in heart disease

4. MYBPC3 mutation carriers had a high frequency of ventricular arrhythmia and syncope. An absence of family history of sudden death (SD) and past history of syncope are useful prognostic factors in patients with hypertrophic cardiomyopathy. MYH7 (zeige MYH7 ELISA Kits) and MYBPC3 mutations did not significantly influence prognosis compared to non-carriers. The patients with the MYBPC3 mutation should be closely followed for the possibility of SD.

5. Replacement Fibrosis was most abundantly present in the hearts with a MYBPC3 mutation that first presented with a Hypertrophic Cardiomyopathy.

6. Mutations in the gene MYBPC3 coding for cardiac myosin-binding protein-C (cMyBP-C), a multi-domain protein, are the most common cause of hypertrophic cardiomyopathy ..This molecular insight suggests that key HCM-causing mutations might significantly modify the native affinity required for the assembly of the domains in cMyBP-C, which is essential for normal cardiac function.

7. Our data demonstrate a critical role of the MLP (zeige MUC2 ELISA Kits)/MyBP-C complex during early myoblast differentiation. Its absence in muscles with mutations or aberrant expression of MLP (zeige MUC2 ELISA Kits) or MyBP-C could be directly implicated in the development of cardiac and skeletal myopathies.

8. Five of the 19 patients (26.3%) had either a pathogenic variant or a likely pathogenic variant in MYBPC3 (n=1), MYH7 (zeige MYH7 ELISA Kits) (n=1), RYR2 (zeige RYR2 ELISA Kits) (n=2), or TNNT2 (zeige TNNT2 ELISA Kits) (n=1). All five variants were missense variants that have been reported previously in patients with channelopathies or cardiomyopathies

9. Double heterozygotes for mutations in DSP (zeige DSP ELISA Kits) and MYBPC3 showed a variable clinical presentation of arrhythmogenic cardiomyopathy and hypertrophic cardiomyopathy.

10. Data provide evidence that MYBPC3 mutations constitute the preeminent cause of hypertrophic cardiomyopathy (HCM) and that they are phenotypically indistinguishable from HCM caused by MYH7 (zeige MYH7 ELISA Kits) mutations.

Rabbit Myosin Binding Protein C, Cardiac (MYBPC3) Interaktionspartner

1. small es, CyrillicMyBP-C modulates interaction of myosin with actin