有哪些信誉好的足球投注网站contributions made by cdc25 phosphatases to proliferation of intestinal epithelial stem and progenitor cells贡献cdc25磷酸酶肠上皮干细胞和祖细胞的增殖.pdfVIP
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contributions made by cdc25 phosphatases to proliferation of intestinal epithelial stem and progenitor cells贡献cdc25磷酸酶肠上皮干细胞和祖细胞的增殖
Contributions Made by CDC25 Phosphatases to Proliferation of Intestinal Epithelial Stem and Progenitor Cells 1¤ 1,2,6 1,2,6 1,3 4 Gwanghee Lee , Sofia Origanti , Lynn S. White , Jinwu Sun , Thaddeus S. Stappenbeck , Helen Piwnica-Worms1,2,5,6* 1 Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri, United States of America, 2 BRIGHT Institute, Washington University School of Medicine, St. Louis, Missouri, United States of America, 3 Molecular Imaging Center, Washington University School of Medicine, St. Louis, Missouri, United States of America, 4 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, United States of America, 5 Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America, 6 Howard Hughes Medical Institute, Chevy Chase, Maryland, United States of America Abstract The CDC25 protein phosphatases drive cell cycle advancement by activating cyclin-dependent protein kinases (CDKs). Humans and mice encode three family members denoted CDC25A, -B and -C and genes encoding these family members can be disrupted individually with minimal phenotypic consequences in adult mice. However, adult mice globally deleted for all three phosphatases die within one week after Cdc25 disruption. A severe loss of absorptive villi due to a failure of crypt epithelial cells to proliferate was observed in the small intestines of these mice. Because the Cdc25s were globally deleted, the small intestinal phenotype and loss of animal viability could not be solely attributed to an intrinsic defect in the inability of small intestinal stem and pro
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