, Assembly Factors Cyclin-Dependent Kinase Inhibitors and Cip / Kip Family of Proteins as Genetic Characterization of the Role of the
暂无分享,去创建一个
M. Barbacid | Alberto Martin | P. Dubus | Antonio Cerqueira | J. Odajima | Catherine E. Symonds | David Santamaríaa
[1] A. Koff,et al. Tyrosine Phosphorylation of the p21 Cyclin-dependent Kinase Inhibitor Facilitates the Development of Proneural Glioma* , 2012, The Journal of Biological Chemistry.
[2] E. Susaki,et al. Common and specific roles of the related CDK inhibitors p27 and p57 revealed by a knock-in mouse model , 2009, Proceedings of the National Academy of Sciences.
[3] C. Cordon-Cardo,et al. Somatic cell type specific gene transfer reveals a tumor-promoting function for p21Waf1/Cip1 , 2007, The EMBO journal.
[4] M. Crosby,et al. Cell Cycle: Principles of Control , 2007, The Yale Journal of Biology and Medicine.
[5] James M. Roberts,et al. Discovery of an oncogenic activity in p27Kip1 that causes stem cell expansion and a multiple tumor phenotype. , 2007, Genes & development.
[6] Richard W. Kriwacki,et al. Cdk-Inhibitory Activity and Stability of p27 Kip1 Are Directly Regulated by Oncogenic Tyrosine Kinases , 2007, Cell.
[7] Tiansen Li,et al. Cyclin D1-dependent kinase activity in murine development and mammary tumorigenesis. , 2006, Cancer cell.
[8] Pierre Dubus,et al. Mammalian Cells Cycle without the D-Type Cyclin-Dependent Kinases Cdk4 and Cdk6 , 2004, Cell.
[9] H. Haapasalo,et al. Cell Cycle Regulators (p21, p53, pRb) in Oligodendrocytic Tumors: a Study by Novel Tumor Microarray Technique , 2001, Journal of Neuro-Oncology.
[10] M. Barbacid,et al. Genetic rescue of Cdk4 null mice restores pancreatic β-cell proliferation but not homeostatic cell number , 2003, Oncogene.
[11] T. Jacks,et al. Acute mutation of retinoblastoma gene function is sufficient for cell cycle re-entry , 2003, Nature.
[12] W. J. Pledger,et al. p27 and p21 Are Not Required for the Formation of Active D Cyclin-cdk4 Complexes , 2003 .
[13] M. Serrano,et al. Tumor susceptibility of p21(Waf1/Cip1)-deficient mice. , 2001, Cancer research.
[14] James M. Roberts,et al. CDK inhibitors: positive and negative regulators of G1-phase progression. , 1999, Genes & development.
[15] James M. Roberts,et al. The p21Cip1 and p27Kip1 CDK ‘inhibitors’ are essential activators of cyclin D‐dependent kinases in murine fibroblasts , 1999, The EMBO journal.
[16] J. Massagué,et al. Differential Interaction of the Cyclin-dependent Kinase (Cdk) Inhibitor p27Kip1 with Cyclin A-Cdk2 and Cyclin D2-Cdk4* , 1997, The Journal of Biological Chemistry.
[17] J. LaBaer,et al. New functional activities for the p21 family of CDK inhibitors. , 1997, Genes & development.
[18] Nobuyuki Shishido,et al. Mice Lacking p27 Kip1 Display Increased Body Size, Multiple Organ Hyperplasia, Retinal Dysplasia, and Pituitary Tumors , 1996, Cell.
[19] James M. Roberts,et al. A Syndrome of Multiorgan Hyperplasia with Features of Gigantism, Tumorigenesis, and Female Sterility in p27 Kip1 -Deficient Mice , 1996, Cell.
[20] K. Manova-Todorova,et al. Enhanced Growth of Mice Lacking the Cyclin-Dependent Kinase Inhibitor Function of p27 Kip1 , 1996, Cell.
[21] A. Deblasio,et al. Formation of p27-CDK complexes during the human mitotic cell cycle. , 1996, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[22] G. Hannon,et al. p21-containing cyclin kinases exist in both active and inactive states. , 1994, Genes & development.
[23] C. Sherr,et al. Regulation of cyclin D-dependent kinase 4 (cdk4) by cdk4-activating kinase , 1994, Molecular and cellular biology.