A key role of the hSNF5/INI1 tumour suppressor in the control of the G1-S transition of the cell cycle
暂无分享,去创建一个
[1] Matthew W. Strobeck,et al. Compensation of BRG-1 Function by Brm , 2002, The Journal of Biological Chemistry.
[2] M. Yaniv,et al. SWI/SNF chromatin remodeling and cancer. , 2002, Current opinion in genetics & development.
[3] G. Kalpana,et al. A masked NES in INI1/hSNF5 mediates hCRM1‐dependent nuclear export: implications for tumorigenesis , 2002, The EMBO journal.
[4] A. Turnell,et al. Adenovirus E1A: remodelling the host cell, a life or death experience , 2001, Oncogene.
[5] O. Delattre,et al. Analysis of the expression of cell cycle regulators in Ewing cell lines: EWS-FLI-1 modulates p57KIP2 and c-Myc expression , 2001, Oncogene.
[6] A. Sands,et al. Disruption of Ini1 Leads to Peri-Implantation Lethality and Tumorigenesis in Mice , 2001, Molecular and Cellular Biology.
[7] C. Roberts,et al. Haploinsufficiency of Snf5 (integrase interactor 1) predisposes to malignant rhabdoid tumors in mice. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[8] M. Yaniv,et al. The murine SNF5/INI1 chromatin remodeling factor is essential for embryonic development and tumor suppression , 2000, EMBO reports.
[9] Weidong Wang,et al. A Specificity and Targeting Subunit of a Human SWI/SNF Family-Related Chromatin-Remodeling Complex , 2000, Molecular and Cellular Biology.
[10] F Randazzo,et al. A Brg1 null mutation in the mouse reveals functional differences among mammalian SWI/SNF complexes. , 2000, Molecular cell.
[11] P. Sudarsanam,et al. The Swi/Snf family nucleosome-remodeling complexes and transcriptional control. , 2000, Trends in genetics : TIG.
[12] Matthew W. Strobeck,et al. BRG-1 is required for RB-mediated cell cycle arrest. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[13] O. Delattre,et al. Mutations of the hSNF5/INI1 gene in renal rhabdoid tumors with second primary brain tumors. , 2000, Journal of the National Cancer Institute.
[14] J. Drake,et al. Familial posterior fossa brain tumors of infancy secondary to germline mutation of the hSNF5 gene. , 2000, American journal of human genetics.
[15] Duanduan Ma,et al. Exit from G1 and S Phase of the Cell Cycle Is Regulated by Repressor Complexes Containing HDAC-Rb-hSWI/SNF and Rb-hSWI/SNF , 2000, Cell.
[16] Weidong Wang,et al. Alteration of hSNF5/INI1/BAF47 detected in rhabdoid cell lines and primary rhabdomyosarcomas but not Wilms' tumors , 1999, Oncogene.
[17] K. Hoang-Xuan,et al. Spectrum of hSNF5/INI1 somatic mutations in human cancer and genotype-phenotype correlations. , 1999, Human molecular genetics.
[18] O. Delattre,et al. Constitutional mutations of the hSNF5/INI1 gene predispose to a variety of cancers. , 1999, American journal of human genetics.
[19] J. Harbour,et al. Cdk Phosphorylation Triggers Sequential Intramolecular Interactions that Progressively Block Rb Functions as Cells Move through G1 , 1999, Cell.
[20] R. Kingston,et al. ATP-dependent remodeling and acetylation as regulators of chromatin fluidity. , 1999, Genes & development.
[21] R. Kingston,et al. Reconstitution of a core chromatin remodeling complex from SWI/SNF subunits. , 1999, Molecular cell.
[22] E. Lees,et al. Cyclin E Associates with BAF155 and BRG1, Components of the Mammalian SWI-SNF Complex, and Alters the Ability of BRG1 To Induce Growth Arrest , 1999, Molecular and Cellular Biology.
[23] M. Kirschner,et al. Mitotic inactivation of a human SWI/SNF chromatin remodeling complex. , 1998, Genes & development.
[24] Olivier Delattre,et al. Truncating mutations of hSNF5/INI1 in aggressive paediatric cancer , 1998, Nature.
[25] Robert A. Weinberg,et al. Functional Inactivation of the Retinoblastoma Protein Requires Sequential Modification by at Least Two Distinct Cyclin-cdk Complexes , 1998, Molecular and Cellular Biology.
[26] S. Srivastava,et al. Effects of adenovirus-mediated p16INK4A expression on cell cycle arrest are determined by endogenous p16 and Rb status in human cancer cells , 1998, Oncogene.
[27] D. Trouche,et al. RB and hbrm cooperate to repress the activation functions of E2F1. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[28] M. Yaniv,et al. Purification and biochemical heterogeneity of the mammalian SWI‐SNF complex. , 1996, The EMBO journal.
[29] Guha,et al. Functional interactions between the hBRM/hBRG1 transcriptional activators and the pRB family of proteins , 1996, Molecular and cellular biology.
[30] D. Trouche,et al. E2F1 and E1A(12S) have a homologous activation domain regulated by RB and CBP. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[31] W. Sellers,et al. Interaction between the retinoblastoma protein and the oncoprotein MDM2 , 1995, Nature.
[32] C. Sardet,et al. A human protein with homology to Saccharomyces cerevisiae SNF5 interacts with the potential helicase hbrm. , 1995, Nucleic acids research.
[33] G. Crabtree,et al. Binding and stimulation of HIV-1 integrase by a human homolog of yeast transcription factor SNF5. , 1994, Science.
[34] Sushovan Guha,et al. The retinoblastoma protein and BRG1 form a complex and cooperate to induce cell cycle arrest , 1994, Cell.
[35] M. Skolnick,et al. A cell cycle regulator potentially involved in genesis of many tumor types. , 1994, Science.
[36] B. Gallie,et al. Transcriptional repression of the E2-containing promoters EIIaE, c-myc, and RB1 by the product of the RB1 gene. , 1992, Molecular and cellular biology.
[37] H. Magdelenat,et al. Breast cancer proliferation measured on cytological samples: a study by flow cytometry of S-phase fractions and BrdU incorporation. , 1991, British Journal of Cancer.
[38] A. Chobanian,et al. Isoform-specific modulation of Na+, K+-ATPase alpha-subunit gene expression in hypertension. , 1988, Science.
[39] J. Biegel,et al. Germ-line and acquired mutations of INI1 in atypical teratoid and rhabdoid tumors. , 1999, Cancer research.
[40] W. Lee,et al. C-terminal truncation of the retinoblastoma gene product leads to functional inactivation. , 1990, Proceedings of the National Academy of Sciences of the United States of America.