Abstract:
:The large T antigen encoded by simian virus 40 (SV40) plays essential roles in the infection of permissive cells, leading to production of progeny virions, and in the infection of nonpermissive cells, leading to malignant transformation. Primary mouse embryo fibroblasts (MEFs) are nonpermissive for SV40, and infection by wild-type SV40 leads to immortalization and transformation of a small percentage of infected cells. We examined the ability of an extensive set of mutants whose lesions affect SV40 large T antigen to immortalize MEFs. We found that immortalization activity was retained by all mutants whose lesions are located upstream of codon 346. This includes a mutant lacking amino acids 168 to 346. We previously showed (M. J. Tevethia, J. M. Pipas, T. Kierstead, and C. Cole, Virology 162:76-89, 1988) that sequences downstream of amino acid 626 are not required for immortalization of primary MEFs. Studies by Thompson et al. (D. L. Thompson, D. Kalderon, A. Smith, and M. Tevethia, Virology 178:15-34, 1990) indicate that all sequences upstream of residue 250, including the domain for binding of tumor suppressor protein Rb, are not required for transformation of MEFs. Together, these studies demonstrate that the immortalization activity of large T antigen for MEFs maps to sequences between 347 and 626. Several mutants with lesions between 347 and 626 retained the ability to immortalize at nearly the wild-type frequency, while others, with small insertions at amino acid 409 or 424 or a deletion of residues 587 to 589, failed to immortalize. The abilities of mutant T antigens to form a complex with tumor suppressor protein p53 were examined. We found that all mutants able to immortalize retained the ability to complex with p53, while all mutants which lost the ability to immortalize were no longer able to bind p53. This suggests that inactivation of the growth-suppressive properties of p53 is essential for immortalization of MEFs.
journal_name
J Viroljournal_title
Journal of virologyauthors
Zhu JY,Abate M,Rice PW,Cole CNdoi
10.1128/JVI.65.12.6872-6880.1991subject
Has Abstractpub_date
1991-12-01 00:00:00pages
6872-80issue
12eissn
0022-538Xissn
1098-5514journal_volume
65pub_type
杂志文章abstract::Syncytial (syn) mutants of herpes simplex virus cause cell fusion. Many syn mutations map to the syn1 locus, which has been identified with the gK (UL53) gene. In this work, the gK genes of eight syn mutants derived from the KOS strain were sequenced to identify residues and, possibly, domains important for the fusion...
journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.68.12.8277-8281.1994
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pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Journal of virology
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.39.2.646-650.1981
更新日期:1981-08-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.80.6.3009-3020.2006
更新日期:2006-03-01 00:00:00
abstract::Nef, an accessory protein of human and simian immunodeficiency viruses, is a critical determinant of pathogenesis that promotes the progression from infection to AIDS. The pathogenic effects of Nef are in large part dependent on its ability to downregulate the macrophage and T-cell coreceptor, CD4. It has been propose...
journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.02725-06
更新日期:2007-04-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/jvi.76.2.499-506.2002
更新日期:2002-01-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.16.3.479-485.1975
更新日期:1975-09-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.69.9.5754-5762.1995
更新日期:1995-09-01 00:00:00
abstract::Highly active antiretroviral therapy (HAART) enables long-term suppression of plasma HIV-1 loads in infected persons, but low-level virus persists and rebounds following cessation of therapy. During HAART, this virus resides in latently infected cells, such as resting CD4(+) T cells, and in other cell types that may s...
journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.02356-09
更新日期:2010-03-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.65.10.5535-5538.1991
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pub_type: 杂志文章
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更新日期:2004-12-01 00:00:00
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更新日期:2006-03-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.8.2.254-256.1971
更新日期:1971-08-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.2.4.365-375.1968
更新日期:1968-04-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2005-10-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.65.3.1400-1407.1991
更新日期:1991-03-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2014-07-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2016-07-27 00:00:00
abstract::The gene encoding glycoprotein F (gF) of herpes simplex virus type 2 (HSV-2) was mapped to the region of the viral genome from 0.62 to 0.64 map units. This region is colinear with, and partially homologous to, the region of the HSV-1 genome previously shown to encode gC. Mapping of the gF gene was done by insertion of...
journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.49.3.741-747.1984
更新日期:1984-03-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2016-09-12 00:00:00
abstract::The Ebola filoviruses are aggressive pathogens that cause severe and often lethal hemorrhagic fever syndromes in humans and nonhuman primates. To date, no effective therapies have been identified. To analyze the entry and fusion properties of Ebola virus, we adapted a human immunodeficiency virus type 1 (HIV-1) virion...
journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.79.2.918-926.2005
更新日期:2005-01-01 00:00:00