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Stem cell depletion through epidermal deletion of Rac1

机译:通过Rac1的表皮删除干细胞

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Mammalian epidermis is maintained by self-renewal of stem cells, but the underlying mechanisms are unknown. Deletion of Rac1, a Rho guanosine triphosphatase, in adult mouse epidermis stimulated stem cells to divide and undergo terminal differentiation, leading to failure to maintain the interfollicular epidermis, hair follicles, and sebaceous glands. Rac1 exerts its effects in the epidermis by negatively regulating c-Myc through p21-activated kinase 2 (PAK2) phosphorylation. We conclude that a pleiotropic regulator of cell adhesion and the cytoskeleton plays a critical role in controlling exit from the stem cell niche and propose that Rac and Myc represent a global stem cell regulatory axis.
机译:哺乳动物表皮是通过干细胞的自我更新来维持的,但其潜在机制尚不清楚。在成年小鼠表皮中Rac鸟苷三磷酸酶Rac1的缺失刺激干细胞分裂并经历终末分化,导致无法维持卵泡间表皮,毛囊和皮脂腺。 Rac1通过p21激活的激酶2(PAK2)磷酸化负调控c-Myc在表皮中发挥作用。我们得出结论,细胞粘附和细胞骨架的多效性调节剂在控制干细胞生态位的退出中起关键作用,并提出Rac和Myc代表了全球干细胞调节轴。

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