440 results on '"Marston, Steven B."'
Search Results
2. Nutraceuticals silybin B, resveratrol, and epigallocatechin-3 gallate-bind to cardiac muscle troponin to restore the loss of lusitropy caused by cardiomyopathy mutations in vitro , in vivo , and in silico.
3. Distinct hypertrophic cardiomyopathy genotypes result in convergent sarcomeric proteoform profiles revealed by top-down proteomics
4. Cardiac physiology
5. Modulation of Structure and Dynamics of Cardiac Troponin by Phosphorylation and Mutations Revealed by Molecular Dynamics Simulations
6. Tropomyosin Must Interact Weakly with Actin to Effectively Regulate Thin Filament Function
7. Mutations in troponin T associated with Hypertrophic Cardiomyopathy increase Ca2+-sensitivity and suppress the modulation of Ca2+-sensitivity by troponin I phosphorylation
8. Instrumentation to study myofibril mechanics from static to artificial simulations of cardiac cycle
9. The Dilated Cardiomyopathy-Causing Mutation ACTC E361G in Cardiac Muscle Myofibrils Specifically Abolishes Modulation of Ca2+ Regulation by Phosphorylation of Troponin I
10. Author Correction: Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes
11. Myosin Regulatory Light Chain (RLC) Phosphorylation Change as a Modulator of Cardiac Muscle Contraction in Disease
12. Z-band Alternatively Spliced PDZ Motif Protein (ZASP) Is the Major O-Linked β-N-Acetylglucosamine-substituted Protein in Human Heart Myofibrils
13. Atomic model of the human cardiac muscle myosin filament
14. The European Muscle Conference 2019 Special Issue
15. Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes
16. Molecular Mechanism of the E99K Mutation in Cardiac Actin (ACTC Gene) That Causes Apical Hypertrophy in Man and Mouse
17. N-Terminal domains of cardiac troponin-I modulate thin filament structure
18. Normal passive viscoelasticity but abnormal myofibrillar force generation in human hypertrophic cardiomyopathy
19. Analysis of cardiac myosin binding protein-C phosphorylation in human heart muscle
20. Thin Filament Control of Uterine Smooth Muscle
21. Uncoupling of myofilament Ca2+ sensitivity from troponin I phosphorylation by mutations can be reversed by epigallocatechin-3-gallate
22. Tropomyosin isoform expression and phosphorylation in the human heart in health and disease
23. How Do Mutations in Contractile Proteins Cause the Primary Familial Cardiomyopathies?
24. Role of Caldesmon in the Ca2+ Regulation of Smooth Muscle Thin Filaments: EVIDENCE FOR A COOPERATIVE SWITCHING MECHANISM
25. Myosin binding protein C phosphorylation in normal, hypertrophic and failing human heart muscle
26. Investigation of changes in skeletal muscle α-actin expression in normal and pathological human and mouse hearts
27. Direct visualisation and kinetic analysis of normal and nemaline myopathy actin polymerisation using total internal reflection microscopy
28. From genotype to phenotype: a longitudinal study of a patient with hypertrophic cardiomyopathy due to a mutation in the MYBPC3 gene
29. Myofilament dysfunction in cardiac disease from mice to men
30. Small heat shock protein Hsp20 (HspB6) as a partner of 14-3-3γ
31. Troponin phosphorylation and regulatory function in human heart muscle: Dephosphorylation of Ser23/24 on troponin I could account for the contractile defect in end-stage heart failure
32. Small heat shock protein with apparent molecular mass 20 kDa (Hsp20, HspB6) is not a genuine actin-binding protein
33. Familial dilated cardiomyopathy mutations uncouple troponin I phosphorylation from changes in myofibrillar Ca2+ sensitivity
34. Myofibrillar Ca2+ sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T
35. The Mechanism of Smooth Muscle Caldesmon-Tropomyosin Inhibition of the Elementary Steps of the Actomyosin ATPase
36. Cardiac myocytes and the cardiac action potential
37. Cardiac physiology
38. Cardiac and skeletal myopathies: can genotype explain phenotype?
39. Structure and properties of K141E mutant of small heat shock protein HSP22 (HspB8, H11) that is expressed in human neuromuscular disorders
40. Introducing a series of topical special issues of the Journal of Muscle Research and Cell Motility: MYBPC3 special issue editorial
41. A novel Ca2+ binding protein associated with caldesmon in Ca2+-regulated smooth muscle thin filaments: evidence for a structurally altered form of calmodulin
42. Titin-truncating mutations associated with dilated cardiomyopathy alter length-dependent activation and its modulation via phosphorylation
43. Approaches to High-Throughput Analysis of Cardiomyocyte Contractility
44. Back to the future: new techniques show that forgotten phosphorylation sites are present in contractile proteins of the heart whilst intensively studied sites appear to be absent
45. The interface between caldesmon domain 4b and subdomain 1 of actin studied by nuclear magnetic resonance spectroscopy
46. The molecular phenotype of human cardiac myosin associated with hypertrophic obstructive cardiomyopathy
47. A simple method for automatic tracking of actin filaments in the motility assay
48. Effect of mutations in the β5–β7 loop on the structure and properties of human small heat shock protein HSP22 (HspB8, H11)
49. Structure-activity studies of the regulatory interaction of the 10 kilodalton c-terminal fragment of caldesmon with actin and the effect of mutation of caldesmon residues 691-696
50. Filamin and gelsolin influence Ca2+-sensitivity of smooth muscle thin filaments
Catalog
Books, media, physical & digital resources
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.