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J Biol Chem. 2003 Feb 7;278(6):4015-20. Epub 2002 Nov 21.

Absence of p21CIP rescues myogenic progenitor cell proliferative and regenerative capacity in Foxk1 null mice.

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1
Departments of Internal Medicine and Molecular Biology, University of Texas Southwestern Medical Center, Dallas 75390-8573, USA.

Abstract

Foxk1 is a forkhead/winged helix transcription factor that is restricted to myogenic progenitor cells in adult skeletal muscle. Mice lacking Foxk1 (Foxk1-/-) display growth retardation and a severe impairment in skeletal muscle regeneration following injury. Here we show that myogenic progenitor cells from Foxk1-/- mice are reduced in number and have perturbed cell cycle progression (G(0)/G(1) arrest). Molecular analysis of Foxk1-/- myogenic progenitor cells revealed increased expression of the cyclin-dependent kinase inhibitor, p21(CIP), independent of changes in other cell cycle inhibitors, including p53. Combinatorial mating of Foxk1-/- mice with p21(CIP)-/- mice, to generate double mutant progeny, resulted in a complete restoration of the growth deficit, skeletal muscle regeneration, myogenic progenitor cell number, and cell cycle progression that characterized the Foxk1-/- mice. We conclude that Foxk1 is essential for regulating cell cycle progression in the myogenic progenitor cell and that the cyclin-dependent kinase inhibitor, p21(CIP), may be a downstream target of Foxk1.

PMID:
12446708
DOI:
10.1074/jbc.M209200200
[Indexed for MEDLINE]
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