p19ARF targets certain E2F species for degradation
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David M. Livingston | Fabio Martelli | Ronald A. DePinho | R. DePinho | N. Sharpless | D. Livingston | S. Grossman | N. Bardeesy | F. Martelli | D. Silver | Nabeel Bardeesy | Daniel P. Silver | Norman E. Sharpless | Steven R. Grossman | Timothy Hamilton | Mihail Rokas | Mihail Rokas | Timothy Hamilton
[1] H. Land,et al. Advanced mammalian gene transfer: high titre retroviral vectors with multiple drug selection markers and a complementary helper-free packaging cell line. , 1990, Nucleic acids research.
[2] D. Beach,et al. p16INK4A and p19ARF act in overlapping pathways in cellular immortalization , 2000, Nature Cell Biology.
[3] F. Martelli,et al. MyoD induces retinoblastoma gene expression during myogenic differentiation. , 1994, Oncogene.
[4] R. Honda,et al. Association of p19ARF with Mdm2 inhibits ubiquitin ligase activity of Mdm2 for tumor suppressor p53 , 1999, The EMBO journal.
[5] J. Trimarchi,et al. E2F-6, a member of the E2F family that can behave as a transcriptional repressor. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[6] S. Lowe,et al. E1A signaling to p53 involves the p19(ARF) tumor suppressor. , 1998, Genes & development.
[7] K. Helin,et al. The E2F transcription factors: key regulators of cell proliferation. , 2000, Biochimica et biophysica acta.
[8] E. Flemington,et al. Regulation of E2F through ubiquitin-proteasome-dependent degradation: stabilization by the pRB tumor suppressor protein. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[9] K. Helin,et al. Phosphorylation of a specific cdk site in E2F-1 affects its electrophoretic mobility and promotes pRB-binding in vitro. , 1995, Oncogene.
[10] K Kornfeld,et al. Multiple docking sites on substrate proteins form a modular system that mediates recognition by ERK MAP kinase. , 1999, Genes & development.
[11] D. Livingston,et al. The retinoblastoma gene product protects E2F-1 from degradation by the ubiquitin-proteasome pathway. , 1996, Genes & development.
[12] 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.
[13] C. Prives,et al. The p53 pathway , 1999, The Journal of pathology.
[14] D. Livingston,et al. Binding and modulation of p53 by p300/CBP coactivators , 1997, Nature.
[15] P. Chambon,et al. Cloning of cDNA sequences of hormone-regulated genes from the MCF-7 human breast cancer cell line. , 1982, Nucleic acids research.
[16] Guillermina Lozano,et al. Rescue of early embryonic lethality in mdm2-deficient mice by deletion of p53 , 1995, Nature.
[17] A. Levine,et al. The high levels of p53 present in adenovirus early region 1-transformed human cells do not cause up-regulation of MDM2 expression. , 1995, Virology.
[18] J. Nevins,et al. E2F3 activity is regulated during the cell cycle and is required for the induction of S phase. , 1998, Genes & development.
[19] C. Blattner,et al. Transcription Factor E2F-1 Is Upregulated in Response to DNA Damage in a Manner Analogous to That of p53 , 1999, Molecular and Cellular Biology.
[20] B. Vogelstein,et al. Mutant p53 DNA clones from human colon carcinomas cooperate with ras in transforming primary rat cells: a comparison of the "hot spot" mutant phenotypes. , 1990, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[21] D. Lane,et al. An N-terminal p14ARF peptide blocks Mdm2-dependent ubiquitination in vitro and can activate p53 in vivo , 2000, Oncogene.
[22] A. Shvarts,et al. Degradation of E2F by the ubiquitin-proteasome pathway: regulation by retinoblastoma family proteins and adenovirus transforming proteins. , 1996, Genes & development.
[23] Wilhelm Krek,et al. Negative regulation of the growth-promoting transcription factor E2F-1 by a stably bound cyclin A-dependent protein kinase , 1994, Cell.
[24] L. Chin,et al. Cooperative effects of INK4a and ras in melanoma susceptibility in vivo. , 1997, Genes & development.
[25] Charles J. Sherr,et al. Nucleolar Arf sequesters Mdm2 and activates p53 , 1999, Nature Cell Biology.
[26] K. Tsai,et al. Mutation of E2f-1 suppresses apoptosis and inappropriate S phase entry and extends survival of Rb-deficient mouse embryos. , 1998, Molecular cell.
[27] J. Trimarchi,et al. E2f3 is critical for normal cellular proliferation. , 2000, Genes & development.
[28] S. Lowe,et al. INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53. , 1999, Genes & development.
[29] M. Roussel,et al. Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis. , 1999, Genes & development.
[30] Ken Chen,et al. The Ink4a Tumor Suppressor Gene Product, p19Arf, Interacts with MDM2 and Neutralizes MDM2's Inhibition of p53 , 1998, Cell.
[31] J L Cleveland,et al. Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization. , 1998, Genes & development.
[32] K. Helin,et al. E2F-6: a novel member of the E2F family is an inhibitor of E2F-dependent transcription , 1998, Oncogene.
[33] C. Sherr,et al. Tumor surveillance via the ARF-p53 pathway. , 1998, Genes & development.
[34] D. Livingston,et al. Unusual proliferation arrest and transcriptional control properties of a newly discovered E2F family member, E2F-6. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[35] Richard A. Ashmun,et al. Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19 ARF , 1997, Cell.
[36] R. DePinho,et al. The INK4A/ARF locus and its two gene products. , 1999, Current opinion in genetics & development.
[37] Goberdhan P Dimri,et al. Regulation of a Senescence Checkpoint Response by the E2F1 Transcription Factor and p14ARF Tumor Suppressor , 2000, Molecular and Cellular Biology.
[38] Chin-Lee Wu,et al. Nuclear localization of DP and E2F transcription factors by heterodimeric partners and retinoblastoma protein family members. , 1996, Journal of cell science.
[39] M. Roussel,et al. p53-independent functions of the p19(ARF) tumor suppressor. , 2000, Genes & development.
[40] 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.
[41] M. Scheffner,et al. Interaction between ubiquitin–protein ligase SCFSKP2 and E2F-1 underlies the regulation of E2F-1 degradation , 1999, Nature Cell Biology.
[42] Karen H. Vousden,et al. p14ARF links the tumour suppressors RB and p53 , 1998, Nature.
[43] J. Herman,et al. Inactivation of the INK4A/ARF locus frequently coexists with TP53 mutations in non-small cell lung cancer , 1999, Oncogene.
[44] A. Levine,et al. P19(ARF) stabilizes p53 by blocking nucleo-cytoplasmic shuttling of Mdm2. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[45] A. Jochemsen,et al. Distinct modulation of p53 activity in transcription and cell-cycle regulation by the large (54 kDa) and small (21 kDa) adenovirus E1B proteins. , 1995, Virology.
[46] D. Livingston,et al. Regulation of endogenous E2F1 stability by the retinoblastoma family proteins. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[47] J. Nevins,et al. E2F1-specific induction of apoptosis and p53 accumulation, which is blocked by Mdm2. , 1998, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[48] R. Mulligan,et al. A stable human-derived packaging cell line for production of high titer retrovirus/vesicular stomatitis virus G pseudotypes. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[49] Y. Xiong,et al. Mutations in human ARF exon 2 disrupt its nucleolar localization and impair its ability to block nuclear export of MDM2 and p53. , 1999, Molecular cell.
[50] D. Livingston,et al. Endogenous E2F-1 promotes timely G0 exit of resting mouse embryo fibroblasts. , 1998, Proceedings of the National Academy of Sciences of the United States of America.