Tumor suppression by Ink4a-Arf: progress and puzzles.
暂无分享,去创建一个
[1] D. Beach,et al. p16INK4A and p19ARF act in overlapping pathways in cellular immortalization , 2000, Nature Cell Biology.
[2] R. DePinho,et al. The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus , 1999, Nature.
[3] A. V. van Rossum,et al. Ablation of the retinoblastoma gene family deregulates G(1) control causing immortalization and increased cell turnover under growth-restricting conditions. , 2000, Genes & development.
[4] D. Carrasco,et al. Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis , 2001, Nature.
[5] K. Helin,et al. Suppression of the p53- or pRB-mediated G1 checkpoint is required for E2F-induced S-phase entry , 2002, Nature Genetics.
[6] J. Shay,et al. When Do Telomeres Matter? , 2001, Science.
[7] Richard A. Ashmun,et al. Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19 ARF , 1997, Cell.
[8] James M. Roberts,et al. A new pathway for mitogen-dependent Cdk2 regulation uncovered in p27Kip1-deficient cells , 1999, Current Biology.
[9] L. Kedes,et al. Twist is a potential oncogene that inhibits apoptosis. , 1999, Genes & development.
[10] T. Kiyono,et al. Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells , 1998, Nature.
[11] D. Hanahan. Cancer: Benefits of bad telomeres , 2000, Nature.
[12] M. Serrano,et al. Murine fibroblasts lacking p21 undergo senescence and are resistant to transformation by oncogenic Ras , 1999, Oncogene.
[13] Marc J. van de Vijver,et al. Senescence bypass screen identifies TBX2, which represses Cdkn2a (p19ARF) and is amplified in a subset of human breast cancers , 2000, Nature Genetics.
[14] H. Varmus,et al. Modeling mutations in the G1 arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a-ARF induces hyperploidy in cultured mouse astrocytes. , 1998, Genes & development.
[15] R. Alani,et al. Id1 regulation of cellular senescence through transcriptional repression of p16/Ink4a , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[16] M. Roussel,et al. p53-independent functions of the p19(ARF) tumor suppressor. , 2000, Genes & development.
[17] A. Smogorzewska,et al. Different telomere damage signaling pathways in human and mouse cells , 2002, The EMBO journal.
[18] J. Shay,et al. Telomere dynamics in cancer progression and prevention: fundamental differences in human and mouse telomere biology , 2000, Nature Medicine.
[19] L. Mayo,et al. A phosphatidylinositol 3-kinase/Akt pathway promotes translocation of Mdm2 from the cytoplasm to the nucleus , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[20] T. Jacks,et al. Targeted disruption of the three Rb-related genes leads to loss of G(1) control and immortalization. , 2000, Genes & development.
[21] R. DePinho,et al. Cellular Senescence Minireview Mitotic Clock or Culture Shock? , 2000, Cell.
[22] Chyung-Ru Wang,et al. Helper T cell differentiation is controlled by the cell cycle. , 1998, Immunity.
[23] F. Zindy,et al. The Arf tumor suppressor gene promotes hyaloid vascular regression during mouse eye development , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[24] S. Lowe,et al. Oncogenic ras activates the ARF-p53 pathway to suppress epithelial cell transformation , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[25] 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.
[26] F. McCormick,et al. Opposing Effects of Ras on p53 Transcriptional Activation of mdm2 and Induction of p19ARF , 2000, Cell.
[27] Karen H. Vousden,et al. p14ARF links the tumour suppressors RB and p53 , 1998, Nature.
[28] Lynda Chin,et al. Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice , 2000, Nature.
[29] G. Peters,et al. INK4a‐deficient human diploid fibroblasts are resistant to RAS‐induced senescence , 2002, The EMBO journal.
[30] S. Shen-Orr,et al. Network motifs in the transcriptional regulation network of Escherichia coli , 2002, Nature Genetics.
[31] R. Bernards,et al. E2F transcriptional repressor complexes are critical downstream targets of p19(ARF)/p53-induced proliferative arrest. , 2002, Cancer cell.
[32] C. Korgaonkar,et al. The alternative reading frame tumor suppressor inhibits growth through p21-dependent and p21-independent pathways. , 2001, Cancer research.
[33] A. Lloyd,et al. Lack of Replicative Senescence in Cultured Rat Oligodendrocyte Precursor Cells , 2001, Science.
[34] R. DePinho,et al. p16(INK4a) and p53 deficiency cooperate in tumorigenesis. , 2002, Cancer research.
[35] G. Peters,et al. Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence , 2001, Nature.
[36] Soyoung Lee,et al. A Senescence Program Controlled by p53 and p16INK4a Contributes to the Outcome of Cancer Therapy , 2002, Cell.
[37] S. Lowe,et al. Dissecting p53 tumor suppressor functions in vivo. , 2002, Cancer cell.
[38] W. Hahn,et al. Modelling the molecular circuitry of cancer , 2002, Nature Reviews Cancer.
[39] J. Shay,et al. Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions. , 2001, Genes & development.
[40] A. Berns,et al. Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice , 2001, Nature.
[41] R. DePinho,et al. Epidermal growth factor receptor and Ink4a/Arf: convergent mechanisms governing terminal differentiation and transformation along the neural stem cell to astrocyte axis. , 2002, Cancer cell.
[42] L. Chin,et al. Dual Inactivation of RB and p53 Pathways in RAS-Induced Melanomas , 2001, Molecular and Cellular Biology.
[43] E. Wagner,et al. JunB suppresses cell proliferation by transcriptional activation of p16INK4a expression , 2000, The EMBO journal.
[44] M. Roussel,et al. Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis. , 1999, Genes & development.
[45] S. Lowe,et al. INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53. , 1999, Genes & development.
[46] A. Lloyd,et al. Lack of Replicative Senescence in Normal Rodent Glia , 2001, Science.
[47] L. Chin,et al. Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[48] F. Zindy,et al. Differential effects of p19Arf and p16Ink4a loss on senescence of murine bone marrow-derived preB cells and macrophages , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[49] L. Chodosh,et al. Hlx is induced by and genetically interacts with T-bet to promote heritable TH1 gene induction , 2002, Nature Immunology.
[50] K Kornfeld,et al. Multiple docking sites on substrate proteins form a modular system that mediates recognition by ERK MAP kinase. , 1999, Genes & development.
[51] Charles J. Sherr,et al. The INK4a/ARF network in tumour suppression , 2001, Nature Reviews Molecular Cell Biology.
[52] Danielle Hulsman,et al. Genome-wide retroviral insertional tagging of genes involved in cancer in Cdkn2a-deficient mice , 2002, Nature Genetics.
[53] A. Gudkov,et al. Cdk4 disruption renders primary mouse cells resistant to oncogenic transformation, leading to Arf/p53-independent senescence. , 2002, Genes & development.
[54] A. Lenferink,et al. ErbB2/Neu-Induced, Cyclin D1-Dependent Transformation Is Accelerated in p27-Haploinsufficient Mammary Epithelial Cells but Impaired in p27-Null Cells , 2002, Molecular and Cellular Biology.