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

First Author  Hawke TJ Year  2003
Journal  J Biol Chem Volume  278
Issue  6 Pages  4015-20
PubMed ID  12446708 Mgi Jnum  J:81688
Mgi Id  MGI:2449837 Doi  10.1074/jbc.M209200200
Citation  Hawke TJ, et al. (2003) Absence of p21CIP Rescues Myogenic Progenitor Cell Proliferative and Regenerative Capacity in Foxk1 Null Mice. J Biol Chem 278(6):4015-20
abstractText  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.
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