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Simian 40 virus

P., Hubert, M., Decroix, Y. and Sarasin, A. (1986). Deficiency in the catalase activity of Xeroderma pigmentosum cells and simian virus 40 transformed human cell extracts. Cancer Res. 46, 538-544. [Pg.125]

Chalifour, L. E., Wirak, D. O., Hansen, U., Wassarman, P. M., and DePamphilis, M. L. (1987). Cis- and trans-acting sequences required for expression of simian virus 40 genes in mouse oocytes. Genes Dev. 1 1096-1106. [Pg.144]

Paranjpe, M.S. and Boone, C.W. (1972). Delayed hypersensitivity to simian virus 40 tumor cells in BALB/c mice demonstrated by a radioisotopic footpad assay. J. Natl. Cancer Inst. 48 563. [Pg.593]

Reddel RR, Salghetti SE, Willey JC, Ohnuki Y, Ke Y, Gerwin BI, Lechner JF, Harris CC (1993) Development of tumorigenicity in simian virus 40-immortalized human bronchial epithelial cell lines. Cancer Res 53(5) 985-991. [Pg.256]

Wikenheiser KA, Vorbroker DK, Rice WR, Clark JC, Bachurski CJ, Oie HK, Whitsett JA (1993) Production of immortalized distal respiratory epithelial cell lines from surfactant protein C/simian virus 40 large tumor antigen transgenic mice. Proc Natl Acad Sci USA 90(23) 11029-11033... [Pg.279]

Figure 26.1 Immortalization of human cells Cells enter replicative senescence at mortality stage 1 (Ml Hayflick limit) after about 60 population doublings (PD). The protein p 16 accumulates in senescent cells. The simian virus 40 (SV40) large T antigen as well as the human papilloma virus (HPV) type 16-E6 and E7 proteins sequester the retinoblastoma protein (Rb) and/or p53 constitutively releases the transcription factor E2F. E2F induces expression proteins required for progression through Gl/S transition, thus the cells escape cell cycle arrest. At mortality stage 2 (M2), transformed cells must overcome senescence and crisis before they are immortalized. This is likely to involve the activation of telomerase either by the introduction of hTERT cDNA or by a genetic change that activates telomerase. Figure 26.1 Immortalization of human cells Cells enter replicative senescence at mortality stage 1 (Ml Hayflick limit) after about 60 population doublings (PD). The protein p 16 accumulates in senescent cells. The simian virus 40 (SV40) large T antigen as well as the human papilloma virus (HPV) type 16-E6 and E7 proteins sequester the retinoblastoma protein (Rb) and/or p53 constitutively releases the transcription factor E2F. E2F induces expression proteins required for progression through Gl/S transition, thus the cells escape cell cycle arrest. At mortality stage 2 (M2), transformed cells must overcome senescence and crisis before they are immortalized. This is likely to involve the activation of telomerase either by the introduction of hTERT cDNA or by a genetic change that activates telomerase.
Gruenert, D. C., C. B. Basbaum, M. J. Welsh, M. Li, W. E. Finkbeiner, and J. A. Nadel. 1988. Characterization of human tracheal epithelial cells transformed by an origin-defective simian virus 40. Proc Natl Acad Sci USA 85(16) 5951-5. [Pg.629]

Small, M. B., Y. Gluzman, and H. L. Ozer. 1982. Enhanced transformation of human fibroblasts by origin-defective simian virus 40. Nature 296(5858) 671-2. [Pg.632]

Toouli, C. D., L. I. Huschtscha, A. A. Neumann, J. R. Noble, L. M. Colgin, B. Hukku, and R. R. Reddel. 2002. Comparison of human mammary epithelial cells immortalized by simian virus 40 T-Antigen or by the telomerase catalytic subunit. Oncogene 21(1) 128-39. [Pg.633]

Brash, D. E., R. R. Reddel, M. Quanrud, K. Yang, M. P. Farrell, and C. C. Harris. 1987. Strontium phosphate transfection of human cells in primary culture Stable expression of the simian virus 40 large-T-antigen gene in primary human bronchial epithelial cells. Mol Cell Biol 7(5) 2031-4. [Pg.634]

Bocchetta, M., I. Di Resta, A. Powers, R. Fresco, A. Tosolini, J. R. Testa, H. I. Pass, P. Rizzo, and M. Carbone. 2000. Human mesothelial cells are unusually susceptible to simian virus 40-mediated transformation and asbestos cocarcinogenicity. Proc Natl Acad Sci USA 97(18) 10214—9. [Pg.636]

Yanai, N., T. Satoh, S. Kyo, K. Abe, M. Suzuki, and M. Obinata. 1991. A tubule cell line established from transgenic mice harboring temperature-sensitive simian virus 40 large T-antigen gene. Jpn J Cancer Res 82(12) 1344-8. [Pg.638]

Jat, P. S., and P. A. Sharp. 1989. Cell lines established by a temperature-sensitive simian virus 40 large T antigen are growth restricted at the non-permissive temperature. Mol Cell Biol 9 1672-81. [Pg.638]

Ray, S., M. E. Anderson, and P. Tegtmeyer. 1996. Differential interaction of temperature-sensitive simian virus 40 T antigens with tumor suppressors pRb and p53. J Virol 70(10) 7224—7. [Pg.638]

Keller W (1975) Determination of the number of superhehcal turns in simian virus 40 DNA by gel electrophoresis. Proc Natl Acad Sci USA 72 4876-4880... [Pg.25]

McHugh MM, Kuo SR, Walsh-O Beime MH, Liu JS, Melendy T, Beerman TA (1999) Bizelesin, a bifunctional cyclopropylpyrroloindole alkylating agent, inhibits simian virus 40 replication in trans by induction of an inhibitor. Biochemistry 38(35) 11508—11515... [Pg.185]

Woynarowski JM, Beerman TA (1997) Effects of bizelesin (U-77,779), a bifunctional alkylating minor groove binder, on repUcation of genomic and simian virus 40 DNA in BSC-1 cells. Biochim Biophys Acta 1353 50-60... [Pg.191]

Since their discovery in the early 1950s (14,15), caveolae had been considered to be uninteresting static organelles that have no capability for the uptake of particles. However, in the past two decades, caveolae have moved into the focus of many researchers because they seem to play an important role in the uptake of various agents, but this is not without controversy. In 2002, Thomsen et al. published strong evidence that caveolae are static fixed domains that are not involved in endocytosis (16), but it has also been reported that caveolae and caveolin can clearly be internalized—at least after specific stimuli, as shown with simian virus 40 (SV40) (17), or by treatment with okadaic acid (18). [Pg.343]

Pelkmans L, Kartenbeck J, Helenius A. Caveolar endocytosis of simian virus 40 reveals a new two-step vesicular-transport pathway to the ER. Nat Cell Biol 2001 3(5) 473 83. [Pg.373]

Damm EM, Pelkmans L, Kartenbeck J, Mezzacasa A, Kurzchalia T, Helenius A. Clathrin- and caveolin-1-independent endocytosis entry of simian virus 40 into cells devoid of caveolae. J Cell Biol 2005 168(3) 477-488. [Pg.378]

Klug, A. and Travers, A.A. (1989) The helical repeat of nucleosome-wrapped DNA. Cell 56, 10-11. White, J.H. and Bauer, W.R. (1989) The helical repeat of nucleosome-wrapped DNA. Cell 56, 9-10. Germond, J.E., Hirt, B., Oudet, P., Gross-Bellard, M., and Chambon, P. (1975) Folding of the DNA double helix in chromatin-like structures from simian virus 40. Proc. Natl. Acad. Sci. USA 72, 1843-1847. [Pg.69]

Beard, P. (1978) Mobility of histones on the chromosome of simian virus 40. Cell 15, 955-967. Spadafora, C., Oudet, P., and Chambon, P. (1979) Rearrangement of chromatin structure induced by increasing ionic strength and temperature. Eur. J. Biochem. 100, 225-235. [Pg.450]


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Simian immunodeficiency virus

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