Tropomyosin pseudo-phosphorylation results in dilated cardiomyopathy.
tropomyosin
phosphorylation
cardiomyopathy
muscle physiology
transgenic mice
cardiac muscle
casein kinase
myofilament
phosphomimetic
Journal
The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R
Informations de publication
Date de publication:
22 02 2019
22 02 2019
Historique:
received:
13
07
2018
revised:
10
12
2018
pubmed:
21
12
2018
medline:
21
5
2019
entrez:
21
12
2018
Statut:
ppublish
Résumé
Phosphorylation of cardiac sarcomeric proteins plays a major role in the regulation of the physiological performance of the heart. Phosphorylation of thin filament proteins, such as troponin I and T, dramatically affects calcium sensitivity of the myofiber and systolic and diastolic functions. Phosphorylation of the regulatory protein tropomyosin (Tpm) results in altered biochemical properties of contraction; however, little is known about the physiological effect of Tpm phosphorylation on cardiac function. To address the
Identifiants
pubmed: 30567734
pii: S0021-9258(20)39385-6
doi: 10.1074/jbc.RA118.004879
pmc: PMC6393621
doi:
Substances chimiques
Tpm1 protein, mouse
0
Tropomyosin
0
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2913-2923Subventions
Organisme : NHLBI NIH HHS
ID : P01 HL062426
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL081680
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL114940
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128468
Pays : United States
Informations de copyright
© 2019 Rajan et al.
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