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Titolo:
Regulation of MyoD function in the dividing myoblast
Autore:
Wei, Q; Paterson, BM;
Indirizzi:
NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA
Titolo Testata:
FEBS LETTERS
fascicolo: 3, volume: 490, anno: 2001,
pagine: 171 - 178
SICI:
0014-5793(20010216)490:3<171:ROMFIT>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
FIBROBLAST GROWTH-FACTOR; DEPENDENT KINASE-4 CDK4; MUSCLE-SPECIFIC GENES; CELL-CYCLE ARREST; MYOGENIC DIFFERENTIATION; C-JUN; DNA-BINDING; RETINOBLASTOMA PROTEIN; SKELETAL-MUSCLE; D1 GENE;
Keywords:
cell cycle; myogenesis; MyoD; cyclin D1; G1 cyclin-dependent kinase; Rb;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
100
Recensione:
Indirizzi per estratti:
Indirizzo: Paterson, BM NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892 m Lab, NIH, Bethesda, MD 20892 USA
Citazione:
Q. Wei e B.M. Paterson, "Regulation of MyoD function in the dividing myoblast", FEBS LETTER, 490(3), 2001, pp. 171-178

Abstract

Proliferating myoblasts express MyoD, yet no phenotypic markers are activated as long as mitogen levels are sufficient to keep the cells dividing. Depending upon mitogen levels, a decision is made in ct that commits the myoblast to either continue to divide or to exit from the cell cycle and activate terminal differentiation. Ectopic expression of MyoD under the control of the RSV or CMV promoters causes 10T1/2 cells to rapidly exit the cell cycle and differentiate as single myocytes, even in growth medium, whereas expression of MgoD under the weaker SV40 promoter is compatible with proliferation. Coexpression of MyoD and cyclin D1, but not cyclins A, B, E or D3, blocks transactivation of a MyoD responsive reporter. Similarly, transfectionof myoblasts with the cyclin-dependent kinase (cdk) inhibitors p16 and p21supports some muscle-specific gene expression even in growth medium. Takenaltogether, these results suggest cell cycle progression negatively regulates myocyte differentiation, possibly through a mechanism involving the D1 responsive cdks. We review evidence coupling growth status, the cell cycle and myogenesis. We describe a novel mitogen-sensitive mechanism that involves the cyclin D1-dependent direct interaction between the G1 cdks and MyoD in the dividing myoblast, which regulates MyoD function in a mitogen-sensitive manner. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 11:14:20