Fragments of the simian virus 40 transforming gene facilitate transformation of rat embryo cells.
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Molecular characterization and functional expression of the human cardiac gap junction channelExpression of the large T protein of polyoma virus promotes the establishment in culture of "normal" rodent fibroblast cell linesFunctional analysis of human cardiac gap junction channel mutantsIdentification of a region of simian virus 40 large T antigen required for cell transformationSimian virus 40 small tumor antigen and an amino-terminal domain of large tumor antigen share a common transforming functionCytotoxic T-lymphocyte epitope immunodominance in the control of choroid plexus tumors in simian virus 40 large T antigen transgenic mice.Permanent expression of p53 in FR 3T3 rat cells but cell cycle-dependent association with large-T antigen in simian virus 40 transformants.Monoclonal antibodies against simian virus 40 nuclear large T tumour antigen: epitope mapping, papova virus cross-reaction and cell surface stainingPolyomavirus-mediated transformation: a model of multistep carcinogenesis.The biological clock that measures the mitotic life-span of mouse embryo fibroblasts continues to function in the presence of simian virus 40 large tumor antigen.Cellular aging is a critical determinant of primary cell resistance to v-src transformation.Expression of p24, a novel p21Waf1/Cip1/Sdi1-related protein, correlates with measurement of the finite proliferative potential of rodent embryo fibroblasts.Lack of involvement of known oncogenic DNA viruses in Epstein-Barr virus-negative Hodgkin's disease.v-src transformation of rat embryo fibroblasts. Inefficient conversion to anchorage-independent growth involves heterogeneity of primary culturesThe amino-terminal transforming region of simian virus 40 large T and small t antigens functions as a J domain.Modeling Schwann cell diseases in transgenic mice.Induction versus progression of brain tumor development: differential functions for the pRB- and p53-targeting domains of simian virus 40 T antigenUse of transgenic mice reveals cell-specific transformation by a simian virus 40 T-antigen amino-terminal mutant.Polyomavirus large T mutants affected in retinoblastoma protein binding are defective in immortalization.p53 mutations are not selected for in simian virus 40 T-antigen-induced tumors from transgenic miceUniform cell-autonomous tumorigenesis of the choroid plexus by papovavirus large T antigensBeta-globin enhancers target expression of a heterologous gene to erythroid tissues of transgenic mice.Cellular gene expression in papillomas of the choroid plexus from transgenic mice that express the simian virus 40 large T antigen.Hybrid genomes of the polyomaviruses JC virus, BK virus, and simian virus 40: identification of sequences important for efficient transformation.Binding of p53 and p105-RB is not sufficient for oncogenic transformation by a hybrid polyomavirus-simian virus 40 large T antigenRequirement for the simian virus 40 small tumor antigen in tumorigenesis in transgenic miceSimian virus 40 can overcome the antiproliferative effect of wild-type p53 in the absence of stable large T antigen-p53 binding.The T/t common region of simian virus 40 large T antigen contains a distinct transformation-governing sequence.JC virus-simian virus 40 genomes containing heterologous regulatory signals and chimeric early regions: identification of regions restricting transformation by JC virus.The large tumor antigen of simian virus 40 encodes at least two distinct transforming functions.Functional simian virus 40 T antigen is expressed in hybrid cells having finite proliferative potential.Sequences from polyomavirus and simian virus 40 large T genes capable of immortalizing primary rat embryo fibroblastsMutation in the polyomavirus genome that activates the properties of large T associated with neoplastic transformationAbility of a T-antigen transport-defective mutant of simian virus 40 to immortalize primary cells and to complement polyomavirus middle T in tumorigenesis.A recombinant murine retrovirus for simian virus 40 large T cDNA transforms mouse fibroblasts to anchorage-independent growthThe simian virus 40 sequences between 0.169 and 0.423 map units are not essential to immortalize early-passage rat embryo cells.Two classes of transformation-deficient, immortalization-positive simian virus 40 mutants constructed by making three-base insertions in the T antigen gene.Overproduction of protein p53 contributes to simian virus 40-mediated transformation.A fragment of the simian virus 40 early genome can induce tumors in nude mice.The t-unique coding domain is important to the transformation maintenance function of the simian virus 40 small t antigen.
P2860
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P2860
Fragments of the simian virus 40 transforming gene facilitate transformation of rat embryo cells.
description
1982 nî lūn-bûn
@nan
1982年の論文
@ja
1982年学术文章
@wuu
1982年学术文章
@zh-cn
1982年学术文章
@zh-hans
1982年学术文章
@zh-my
1982年学术文章
@zh-sg
1982年學術文章
@yue
1982年學術文章
@zh
1982年學術文章
@zh-hant
name
Fragments of the simian virus ...... formation of rat embryo cells.
@ast
Fragments of the simian virus ...... formation of rat embryo cells.
@en
type
label
Fragments of the simian virus ...... formation of rat embryo cells.
@ast
Fragments of the simian virus ...... formation of rat embryo cells.
@en
prefLabel
Fragments of the simian virus ...... formation of rat embryo cells.
@ast
Fragments of the simian virus ...... formation of rat embryo cells.
@en
P2860
P356
P1476
Fragments of the simian virus ...... formation of rat embryo cells.
@en
P2093
P2860
P304
P356
10.1073/PNAS.79.17.5189
P407
P577
1982-09-01T00:00:00Z