Sakthivel Sadayappan

Novel deletions in MYH7 and MYBPC3 identified in Indian families with familial hypertrophic cardiomyopathy.

In vivo and in vitro analysis of cardiac troponin I phosphorylation.

Transgenic rabbit model for human troponin I-based hypertrophic cardiomyopathy.

Cardiac isoform of alpha-2 macroglobulin--a new biomarker for myocardial infarcted diabetic patients.

Cardiac myosin-binding protein-C phosphorylation and cardiac function.

PKC-betaII sensitizes cardiac myofilaments to Ca2+ by phosphorylating troponin I on threonine-144.

Cardiac myosin binding protein C phosphorylation is cardioprotective.

Novel mitochondrial DNA mutations implicated in Noonan syndrome.

Distribution and structure-function relationship of myosin heavy chain isoforms in the adult mouse heart.

Cardiac transgenic and gene transfer strategies converge to support an important role for troponin I in regulating relaxation in cardiac myocytes.

Role of the acidic N' region of cardiac troponin I in regulating myocardial function.

Control of in vivo left ventricular [correction] contraction/relaxation kinetics by myosin binding protein C: protein kinase A phosphorylation dependent and independent regulation.

The death of transcriptional chauvinism in the control and regulation of cardiac contractility.

A common MYBPC3 (cardiac myosin binding protein C) variant associated with cardiomyopathies in South Asia.

Cardiac myosin binding protein-C phosphorylation in a {beta}-myosin heavy chain background.

Inducible expression of active protein phosphatase-1 inhibitor-1 enhances basal cardiac function and protects against ischemia/reperfusion injury.

Phosphorylation and function of cardiac myosin binding protein-C in health and disease.

Distinct sarcomeric substrates are responsible for protein kinase D-mediated regulation of cardiac myofilament Ca2+ sensitivity and cross-bridge cycling.

Targeted genome-wide enrichment of functional regions.

Analysis of cardiac myosin binding protein-C phosphorylation in human heart muscle.

Novel role for p90 ribosomal S6 kinase in the regulation of cardiac myofilament phosphorylation.

A critical function for Ser-282 in cardiac Myosin binding protein-C phosphorylation and cardiac function.

Roles for cardiac MyBP-C in maintaining myofilament lattice rigidity and prolonging myosin cross-bridge lifetime.

Cardiac myosin binding protein-C is a potential diagnostic biomarker for myocardial infarction.

Unique single molecule binding of cardiac myosin binding protein-C to actin and phosphorylation-dependent inhibition of actomyosin motility requires 17 amino acids of the motif domain.

Contractile dysfunction irrespective of the mutant protein in human hypertrophic cardiomyopathy with normal systolic function.

Structural insight into unique cardiac myosin-binding protein-C motif: a partially folded domain.

Cardiac myosin binding protein-C: a potential early-stage, cardiac-specific biomarker of ischemia-reperfusion injury.

Pathogenic properties of the N-terminal region of cardiac myosin binding protein-C in vitro.

Protein kinase C depresses cardiac myocyte power output and attenuates myofilament responses induced by protein kinase A.

Protein kinase D increases maximal Ca2+-activated tension of cardiomyocyte contraction by phosphorylation of cMyBP-C-Ser315.

Interleukin-10 treatment attenuates pressure overload-induced hypertrophic remodeling and improves heart function via signal transducers and activators of transcription 3-dependent inhibition of nuclear factor-κB.

Cardiac myosin binding protein-C: redefining its structure and function.

In vivo and in vitro cardiac responses to beta-adrenergic stimulation in volume-overload heart failure.

GSK3β phosphorylates newly identified site in the proline-alanine-rich region of cardiac myosin-binding protein C and alters cross-bridge cycling kinetics in human: short communication.

Perturbed length-dependent activation in human hypertrophic cardiomyopathy with missense sarcomeric gene mutations.

Myofilament Ca2+ desensitization mediates positive lusitropic effect of neuronal nitric oxide synthase in left ventricular myocytes from murine hypertensive heart.

Agonist activated PKCβII translocation and modulation of cardiac myocyte contractile function.

Increase in cardiac myosin binding protein-C plasma levels is a sensitive and cardiac-specific biomarker of myocardial infarction.