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Titolo:
ALTERED INTERACTIONS AMONG THIN FILAMENT PROTEINS MODULATE CARDIAC-FUNCTION
Autore:
SOLARO RJ; VANEYK J;
Indirizzi:
UNIV ILLINOIS,COLL MED,DEPT PHYSIOL & BIOPHYS,M-C901,835 S WOLCOTT CHICAGO IL 60612
Titolo Testata:
Journal of Molecular and Cellular Cardiology
fascicolo: 2, volume: 28, anno: 1996,
pagine: 217 - 230
SICI:
0022-2828(1996)28:2<217:AIATFP>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
TROPONIN-TROPOMYOSIN COMPLEX; RABBIT SKELETAL-MUSCLE; AMINO-ACID-SEQUENCE; KINASE-C; SARCOPLASMIC-RETICULUM; MYOSIN SUBFRAGMENT-1; PHOSPHOLAMBAN PHOSPHORYLATION; ALPHA-ADRENOCEPTORS; ACTOMYOSIN MGATPASE; BIOLOGICAL-ACTIVITY;
Keywords:
TROPONIN; TROPOMYOSIN; ACTIN; LENGTH-DEPENDENT ACTIVATION; PHOSPHORYLATION; ISCHEMIA; INOTROPIC AGENTS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
104
Recensione:
Indirizzi per estratti:
Citazione:
R.J. Solaro e J. Vaneyk, "ALTERED INTERACTIONS AMONG THIN FILAMENT PROTEINS MODULATE CARDIAC-FUNCTION", Journal of Molecular and Cellular Cardiology, 28(2), 1996, pp. 217-230

Abstract

The transition of cardiac muscle myofilament activity from the diastolic to the systolic state is a complex allosteric/co-operative process, rich in potential control mechanisms. The rate and intensity of the transition is modulated by the mechanical state of the myofilaments, by covalent and non-covalent mechanisms, and by the isoform population of myofilament proteins, Moreover, the process is altered in pathological states and subject to modification by pharmacological agents with potential use as inotropic drugs, We present here a current perceptionof the process, with focus on molecular interactions of the thin filament components, especially troponin I. Our discussion is couched in terms of what we believe to be pressing questions in the current state of knowledge of this system, These questions are as follows: what is the topology of the thin filament and how do thin filament proteins regulate the activation of cross-bridge cycling! What is the relative role of protein phosphorylation of thin filament proteins in the regulation of the cardiac activity and dynamics! What is the relative role of feedback effects of cross-bridge binding on thin filament activity! Answers to these questions have taken on new significance, with the identification of familial hypertrophic cardiomyopathy as a ''sarcomeric''disease related to missense mutations in myosin, troponin T, and tropomyosin, As discussed, new and exciting developments in this area are bringing us closer to the answers to these questions. (C) 1996 Academic Press Limited

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 11:41:04