Armen O. Simonyan
4 Tikhoretsky Ave
Saint Petersburg, SPE 194064, Russian Federation
Saint Petersburg, SPE 194064, Russian Federation
Last Updated: 09/26/2026
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Found 14 publications
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.
Journal: International journal of molecular sciences
Published: May 12, 2021
Looking for Targets to Restore the Contractile Function in Congenital Myopathy Caused by Gln147Pro Tropomyosin.
Journal: International journal of molecular sciences
Published: August 27, 2020
Combined surgical treatment of a patient with kidney cancer stage 4 and coronary artery disease
Journal: Khirurgiia
Published: August 02, 2020
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.
Journal: International journal of molecular sciences
Published: May 30, 2020
The molecular mechanism of muscle dysfunction associated with the R133W mutation in Tpm2.2.
Journal: Biochemical and biophysical research communications
Published: November 25, 2019
The molecular mechanisms of a high Ca2+-sensitivity and muscle weakness associated with the Ala155Thr substitution in Tpm3.12.
Journal: Biochemical and biophysical research communications
Published: May 17, 2019
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.
Journal: International journal of molecular sciences
Published: October 19, 2018
The reason for the low Ca2+-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.
Journal: Biochemical and biophysical research communications
Published: May 14, 2018
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.
Journal: Biochemical and biophysical research communications
Published: October 25, 2017
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.
Journal: Archives of biochemistry and biophysics
Published: June 26, 2017
Deviations in conformational rearrangements of thin filaments and myosin caused by the Ala155Thr substitution in hydrophobic core of tropomyosin.
Journal: Biochimica et biophysica acta. Proteins and proteomics
Published: May 04, 2017
Last Updated: 09/26/2026