TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
about
The Importance of Intrinsically Disordered Segments of Cardiac Troponin in Modulating Function by Phosphorylation and Disease-Causing MutationsWhy Is there a Limit to the Changes in Myofilament Ca2+-Sensitivity Associated with Myopathy Causing Mutations?Sarcomere Dysfunction in Nemaline Myopathy.Dysfunctional sarcomere contractility contributes to muscle weakness in ACTA1-related nemaline myopathy (NEM3).HCM and DCM cardiomyopathy-linked α-tropomyosin mutations influence off-state stability and crossbridge interaction on thin filaments.
P2860
TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 29 September 2015
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
@en
TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
@nl
type
label
TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
@en
TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
@nl
prefLabel
TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
@en
TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
@nl
P2093
P2860
P50
P356
P1433
P1476
TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.
@en
P2093
A Rutkowski
C G Bönnemann
Cac Ottenheijm
E McNamara
E P Wartchow
J M de Winter
M A Gibbons
P2860
P304
P356
10.1002/ANA.24535
P577
2015-09-29T00:00:00Z