a role for the retinoblastoma protein as a regulator of mouse osteoblast cell adhesion implications for osteogenesis and osteosarcoma formation视网膜母细胞瘤蛋白作为管理者的角色老鼠成骨细胞对骨和骨肉瘤形成细胞粘附的影响.pdfVIP

a role for the retinoblastoma protein as a regulator of mouse osteoblast cell adhesion implications for osteogenesis and osteosarcoma formation视网膜母细胞瘤蛋白作为管理者的角色老鼠成骨细胞对骨和骨肉瘤形成细胞粘附的影响.pdf

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a role for the retinoblastoma protein as a regulator of mouse osteoblast cell adhesion implications for osteogenesis and osteosarcoma formation视网膜母细胞瘤蛋白作为管理者的角色老鼠成骨细胞对骨和骨肉瘤形成细胞粘附的影响

A Role for the Retinoblastoma Protein As a Regulator of Mouse Osteoblast Cell Adhesion: Implications for Osteogenesis and Osteosarcoma Formation ´ 1 2 ´ 1 3 Bernadette Sosa-Garcıa , Volkan Gunduz , Viviana Vazquez-Rivera , W. Douglas Cress , Gabriela 3 3 2 1 Wright , Haikuo Bian , Philip W. Hinds , Pedro G. Santiago-Cardona * 1 Biochemistry Department, Ponce School of Medicine, Ponce, Puerto Rico, 2 Molecular Oncology Research Institute, Tufts Medical Center, Boston, Massachusetts, United States of America, 3 Molecular Oncology and Thoracic Oncology Departments, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, United States of America Abstract The retinoblastoma protein (pRb) is a cell cycle regulator inactivated in most human cancers. Loss of pRb function results from mutations in the gene coding for pRb or for any of its upstream regulators. Although pRb is predominantly known as a cell cycle repressor, our data point to additional pRb functions in cell adhesion. Our data show that pRb regulates the expression of a wide repertoire of cell adhesion genes and regulates the assembly of the adherens junctions required for cell adhesion. We conducted our studies in osteoblasts, which depend on both pRb and on cell-to-cell contacts for their differentiation and function. We generated knockout mice in which the RB gene was excised specifically in osteoblasts using the cre-lox P system and found that osteoblasts from pRb knockout mice did not assemble adherens junction at their membranes. pRb depletion in wild type osteoblasts using RNAi also disrupted adherens junctions. M

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