Loss of the ARF tumor suppressor reverses premature replicative arrest but not radiation hypersensitivity arising from disabled atm function.
暂无分享,去创建一个
F. Zindy | C. Sherr | T. Kamijo | J. Diehl | E. Kamp | E. V. D. van de Kamp | P. Mckinnon | M. J. Chong | Miriam J. Chong
[1] Y Taya,et al. A role for ATR in the DNA damage-induced phosphorylation of p53. , 1999, Genes & development.
[2] P. Leder,et al. Loss of atm radiosensitizes multiple p53 null tissues. , 1998, Cancer research.
[3] J. Qin,et al. The 400 kDa subunit of the PCAF histone acetylase complex belongs to the ATM superfamily. , 1998, Molecular cell.
[4] J R Yates,et al. The ATM-related cofactor Tra1 is a component of the purified SAGA complex. , 1998, Molecular cell.
[5] C. Prives. Signaling to p53 Breaking the MDM2–p53 Circuit , 1998, Cell.
[6] A. Giaccia,et al. The complexity of p53 modulation: emerging patterns from divergent signals. , 1998, Genes & development.
[7] C. Sherr,et al. Tumor surveillance via the ARF-p53 pathway. , 1998, Genes & development.
[8] Y Taya,et al. Activation of the ATM kinase by ionizing radiation and phosphorylation of p53. , 1998, Science.
[9] Y. Shiloh,et al. ATM: from gene to function. , 1998, Human molecular genetics.
[10] Kevin Ryan,et al. The alternative product from the human CDKN2A locus, p14ARF, participates in a regulatory feedback loop with p53 and MDM2 , 1998, The EMBO journal.
[11] M. Cole,et al. The Novel ATM-Related Protein TRRAP Is an Essential Cofactor for the c-Myc and E2F Oncoproteins , 1998, Cell.
[12] J L Cleveland,et al. Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization. , 1998, Genes & development.
[13] S. Lowe,et al. E1A signaling to p53 involves the p19(ARF) tumor suppressor. , 1998, Genes & development.
[14] F. Zindy,et al. Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[15] J. Morgan,et al. Requirement for Atm in ionizing radiation-induced cell death in the developing central nervous system. , 1998, Science.
[16] Nucleo-cytoplasmic shuttling of the hdm2 oncoprotein regulates the levels of the p53 protein via a pathway used by the human immunodeficiency virus rev protein. , 1998, The EMBO journal.
[17] Ken Chen,et al. The Ink4a Tumor Suppressor Gene Product, p19Arf, Interacts with MDM2 and Neutralizes MDM2's Inhibition of p53 , 1998, Cell.
[18] Yue Xiong,et al. ARF Promotes MDM2 Degradation and Stabilizes p53: ARF-INK4a Locus Deletion Impairs Both the Rb and p53 Tumor Suppression Pathways , 1998, Cell.
[19] Y Taya,et al. Enhanced phosphorylation of p53 by ATM in response to DNA damage. , 1998, Science.
[20] S. Schreiber,et al. Overexpression of a kinase‐inactive ATR protein causes sensitivity to DNA‐damaging agents and defects in cell cycle checkpoints , 1998, The EMBO journal.
[21] P. Leder,et al. Loss of p21 increases sensitivity to ionizing radiation and delays the onset of lymphoma in atm-deficient mice. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[22] Hirofumi Tanaka,et al. Oncoprotein MDM2 is a ubiquitin ligase E3 for tumor suppressor p53 , 1997, FEBS letters.
[23] Y Taya,et al. DNA damage induces phosphorylation of the amino terminus of p53. , 1997, Genes & development.
[24] Richard A. Ashmun,et al. Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19 ARF , 1997, Cell.
[25] Yoichi Taya,et al. DNA Damage-Induced Phosphorylation of p53 Alleviates Inhibition by MDM2 , 1997, Cell.
[26] María A Blasco,et al. Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA , 1997, Cell.
[27] T. Davison,et al. ATM‐dependent telomere loss in aging human diploid fibroblasts and DNA damage lead to the post‐translational activation of p53 protein involving poly(ADP‐ribose) polymerase , 1997, The EMBO journal.
[28] P. Leder,et al. atm and p53 cooperate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity , 1997, Nature Genetics.
[29] F. Zindy,et al. Expression of the p16INK4a tumor suppressor versus other INK4 family members during mouse development and aging , 1997, Oncogene.
[30] Stephen N. Jones,et al. Regulation of p53 stability by Mdm2 , 1997, Nature.
[31] M. Oren,et al. Mdm2 promotes the rapid degradation of p53 , 1997, Nature.
[32] P. Leder,et al. Genetic interactions between atm and p53 influence cellular proliferation and irradiation-induced cell cycle checkpoints. , 1997, Cancer research.
[33] A. Levine. p53, the Cellular Gatekeeper for Growth and Division , 1997, Cell.
[34] Y. Shiloh,et al. The genetic defect in ataxia-telangiectasia. , 1997, Annual review of immunology.
[35] G. Hannon,et al. Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[36] P. Leder,et al. Pleiotropic defects in ataxia-telangiectasia protein-deficient mice. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[37] D. Baltimore,et al. Dual roles of ATM in the cellular response to radiation and in cell growth control. , 1996, Genes & development.
[38] Francis Collins,et al. Atm-Deficient Mice: A Paradigm of Ataxia Telangiectasia , 1996, Cell.
[39] S. Benchimol,et al. From telomere loss to p53 induction and activation of a DNA-damage pathway at senescence: The telomere loss/DNA damage model of cell aging , 1996, Experimental Gerontology.
[40] G. Peters,et al. Regulation of p16CDKN2 expression and its implications for cell immortalization and senescence , 1996, Molecular and cellular biology.
[41] F. Zindy,et al. Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest , 1995, Cell.
[42] R. DePinho,et al. Inhibition of ras-induced proliferation and cellular transformation by p16INK4 , 1995, Science.
[43] N. Hay,et al. Myc-mediated apoptosis requires wild-type p53 in a manner independent of cell cycle arrest and the ability of p53 to induce p21waf1/cip1. , 1994, Genes & development.
[44] H. Hermeking,et al. Mediation of c-Myc-induced apoptosis by p53. , 1994, Science.
[45] D. Housman,et al. Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[46] David Beach,et al. p21 is a universal inhibitor of cyclin kinases , 1993, Nature.
[47] G. Hannon,et al. A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4 , 1993, Nature.
[48] K. Khanna,et al. Ionizing radiation and UV induction of p53 protein by different pathways in ataxia-telangiectasia cells. , 1993, Oncogene.
[49] J. Trent,et al. WAF1, a potential mediator of p53 tumor suppression , 1993, Cell.
[50] S. Elledge,et al. The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases , 1993, Cell.
[51] Bert Vogelstein,et al. Oncoprotein MDM2 conceals the activation domain of tumour suppressor p53 , 1993, Nature.
[52] S. Lowe,et al. Stabilization of the p53 tumor suppressor is induced by adenovirus 5 E1A and accompanies apoptosis. , 1993, Genes & development.
[53] B. Vogelstein,et al. A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia , 1992, Cell.
[54] A. Levine,et al. The mdm-2 oncogene product forms a complex with the p53 protein and inhibits p53-mediated transactivation , 1992, Cell.
[55] R. Weinberg,et al. Cellular oncogenes and multistep carcinogenesis. , 1983, Science.
[56] H. Ruley. Adenovirus early region 1A enables viral and cellular transforming genes to transform primary cells in culture , 1983, Nature.
[57] Y. Shiloh,et al. Colony-forming ability of ataxia-telangiectasia skin fibroblasts is an indicator of their early senescence and increased demand for growth factors. , 1982, Experimental cell research.