153 results on '"Borovikov, Yurii S."'
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2. Molecular Mechanisms of Deregulation of Muscle Contractility Caused by the R168H Mutation in TPM3 and Its Attenuation by Therapeutic Agents
3. Myopathy-causing Q147P TPM2 mutation shifts tropomyosin strands further towards the open position and increases the proportion of strong-binding cross-bridges during the ATPase cycle
4. The effect of the Asp175Asn and Glu180Gly TPM1 mutations on actin–myosin interaction during the ATPase cycle
5. Modulation of the effects of tropomyosin on actin and myosin conformational changes by troponin and Ca 2+
6. Molecular Mechanisms of the Deregulation of Muscle Contraction Induced by the R90P Mutation in Tpm3.12 and the Weakening of This Effect by BDM and W7
7. Twitchin of mollusc smooth muscles can induce “catch”-like properties in human skeletal muscle: support for the assumption that the “catch” state involves twitchin linkages between myofilaments
8. Looking for Targets to Restore the Contractile Function in Congenital Myopathy Caused by Gln147Pro Tropomyosin
9. Molecular Mechanisms of Muscle Weakness Associated with E173A Mutation in Tpm3.12. Troponin Ca2+ Sensitivity Inhibitor W7 Can Reduce the Damaging Effect of This Mutation
10. The molecular mechanism of muscle dysfunction associated with the R133W mutation in Tpm2.2
11. Conformational Analysis of Mutant Proteins as a Tool for Classification of Myopathies
12. Behavior of caldesmon upon interaction of thin filaments with myosin subfragment 1 in ghost fibers
13. Conformational Changes of Contractile Proteins and Their Role in Muscle Contraction
14. The molecular mechanisms of a high Ca2+-sensitivity and muscle weakness associated with the Ala155Thr substitution in Tpm3.12
15. The reason for the low Ca 2+ -sensitivity of thin filaments associated with the Glu41Lys mutation in the TPM2 gene is “freezing” of tropomyosin near the outer domain of actin and inhibition of actin monomer switching off during the ATPase cycle
16. The primary cause of muscle disfunction associated with substitutions E240K and R244G in tropomyosin is aberrant behavior of tropomyosin and response of actin and myosin during ATPase cycle
17. Molecular mechanisms of dysfunction of muscle fibres associated with Glu139 deletion in TPM2 gene
18. The reason for a high Ca2+-sensitivity associated with Arg91Gly substitution in TPM2 gene is the abnormal behavior and high flexibility of tropomyosin during the ATPase cycle
19. Molecular mechanisms of deregulation of the thin filament associated with the R167H and K168E substitutions in tropomyosin Tpm1.1
20. Linking the Glu150Ala mutation in slow skeletal muscle Tpm3.12 to congenital myopathy
21. Abnormal movement of tropomyosin and response of myosin heads and actin during the ATPase cycle caused by the Arg167His, Arg167Gly and Lys168Glu mutations in TPM1 gene
22. Aberrant movement of β-tropomyosin associated with congenital myopathy causes defective response of myosin heads and actin during the ATPase cycle
23. The E117K mutation in β-tropomyosin disturbs concerted conformational changes of actomyosin in muscle fibers
24. Gly126Arg substitution causes anomalous behaviour of α-skeletal and β-smooth tropomyosins during the ATPase cycle
25. The nemaline myopathy-causing E117K mutation in β-tropomyosin reduces thin filament activation
26. Twitchin can regulate the ATPase cycle of actomyosin in a phosphorylation-dependent manner in skinned mammalian skeletal muscle fibres
27. The effect of the dilated cardiomyopathy-causing Glu40Lys TPM1 mutation on actin-myosin interactions during the ATPase cycle
28. Hypertrophic cardiomyopathy-causing Asp175asn and Glu180gly Tpm1 mutations shift tropomyosin strands further towards the open position during the ATPase cycle
29. Molluscan twitchin can control actin–myosin interaction during ATPase cycle
30. A new property of twitchin to restrict the “rolling” of mussel tropomyosin and decrease its affinity for actin during the actomyosin ATPase cycle
31. Caldesmon inhibits the rotation of smooth actin subdomain-1 and alters its mobility during the ATP hydrolysis cycle
32. The effect of the dilated cardiomyopathy-causing mutation Glu54Lys of α-tropomyosin on actin–myosin interactions during the ATPase cycle
33. Dilated cardiomyopathy mutations in α-tropomyosin inhibit its movement during the ATPase cycle
34. Caldesmon inhibits the actin–myosin interaction by changing its spatial orientation and mobility during the ATPase activity cycle
35. Caldesmon restricts the movement of both C- and N-termini of tropomyosin on F-actin in ghost fibers during the actomyosin ATPase cycle
36. Caldesmon freezes the structure of actin filaments during the actomyosin ATPase cycle
37. Proteolytic cleavage of actin within the DNase-I-binding loop changes the conformation of F-actin and its sensitivity to myosin binding
38. Calcium modulates conformational changes in F-actin induced by smooth muscle heavy meromyosin
39. Effects of denervation and muscle inactivity on the organization of F-actin
40. Comparison of the Effects of Calponin and a 38-kDa Caldesmon Fragment on Formation of the “Strong-Binding” State in Ghost Muscle Fibers
41. The effect of Ca2+ on the conformation of tropomyosin and actin in regulated actin filaments with or without bound myosin subfragment 1
42. Troponin I and caldesmon restrict alterations in actin structure occurring on binding of myosin subfragment I
43. Caldesmon inhibits both force development and transition of actin monomers from “OFF” to “ON” conformational state by changing its position in thin filaments
44. The shortening of the N-terminus of myosin essential light chain A1 influences the interaction of heavy meromyosin with actin.
45. The effect of myosin light chain phosphorylation and Mg2+ on the conformation of myosin in thick filaments of glycerinated fibers of rabbit skeletal muscle.
46. Effect of troponin-tropomyosin complex and Ca2+ on conformational changes in F-actin induced by myosin subfragment-1.
47. Effect of Ca2+ Binding to 5,5 -Dithiobis(2-nitrobenzoic acid) Light Chains on Conformational Changes of F-Actin Caused by Myosin Subfragment-1.
48. Interaction of Tropomyosin with F-Actin-Heavy Meromyosin Complex.
49. Secretion from permeabilised mast cells is enhanced by addition of gelsolin: contrasting effects of endogenous gelsolin
50. The Primary Causes of Muscle Dysfunction Associated with the Point Mutations in Tpm3.12; Conformational Analysis of Mutant Proteins as a Tool for Classification of Myopathies.
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