Adenovirus type 12-transformed rat embryo brain and rat liver epithelial cell lines: adenovirus type 12 genome content and viral protein expression

Paraskeva, Christos; Brown, Keith; Dunn, Ashley R.; Gallimore, Phillip H.

doi:10.1128/jvi.44.2.759-764.1982

Cited by 12 publications

(1 citation statement)

References 38 publications

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“…RFC1 is an Adl2-transformed Hooded Lister rat kidney cell line (39). Adl2 100.1 is an Adl2-transformed cell line (40). 5A12 is a BRK cell line transformed with a recombinant AdS virus expressing Adl2 E1A and AdS E1B (11).…”

Section: Dna Sequencingmentioning

confidence: 99%

Adenovirus 12-mediated down-regulation of the major histocompatibility complex (MHC) class I promoter: identification of a negative regulatory element responsive to Ad12 E1A

1994

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In highly oncogenic adenovirus (Ad) 12-transformed cells, major histocompatibility complex (MHC) class I gene expression is down-regulated by the products of the viral E1A oncogene at the level of initiation of transcription. However, class I gene expression is unaltered or elevated in non-oncogenic Ad2- or Ad5-transformed cells. These changes in class I expression may permit Ad12-transformed cells to escape host immune surveillance and elicit tumour formation. Here we show that the 2kb of 5' flanking region of the mouse H-2Kb class I gene is sufficient to mediate down-regulation of transcription driven from homologous or heterologous (HSV thymidine kinase) basal promoter elements in cells expressing Ad12 E1A, but not in Ad2 E1A-expressing cells. Deletion analysis of the 2kb region showed that sequences from -1.18 to -1.44kb (relative to the cap site) were a target for Ad12 E1A-mediated transcriptional down-regulation. Deletion of this entire region from the 2kb flanking sequence of the H-2Kb gene abolished Ad12 E1A-mediated down-regulation of transcription. Computer analysis of the -1.18 to -1.44kb sequence identified two 6/7bp matches with the AP-1 transcription factor consensus sequence and two matches with the pig MHC class I PD1 repressor element. Gel retardation analysis using overlapping DNA fragments derived from the -1.18 to -1.44kb sequence revealed several DNA:protein complexes formed using nuclear extract derived from Ad12-, but not from Ad2- or Ad5-transformed cells. Some of these DNA:protein complexes were also present, but at lower levels, in nuclear extracts from untransformed rat cells suggesting the possible involvement of cellular factors in the mechanism of down-regulation mediated by Ad12 E1A. A binding site for the AP-1 factor failed to compete for protein binding to fragments within the -1.18 to -1.44 sequence, while the PD1 site competed for binding only in the -1.15 to -1.23 region. These results indicate that novel factors (as well as a previously identified class I repressor, PD1) may be involved in Ad12 E1A-mediated down-regulation of MHC class I transcription.

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Section: Dna Sequencingmentioning

confidence: 99%

Adenovirus 12-mediated down-regulation of the major histocompatibility complex (MHC) class I promoter: identification of a negative regulatory element responsive to Ad12 E1A

1994

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Cellular proteins expressed in herpes simplex virus transformed cells also accumulate on herpes simplex virus infection.

Macnab¹,

Orr²,

Thangue³

1985

The EMBO Journal

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The cell proteins expressed in rat embryo cells transformed by herpes simplex virus (HSV) have been analysed by immunoprecipitation assays to determine those polypeptides which can be identified by immunoprecipitation with the sera of tumour‐bearing animals and also with antisera to herpes simplex infected cells. Cell polypeptides commonly recognised by both these sera have been further characterised using a monoclonal antibody directed against a cellular polypeptide which accumulates on HSV‐2 lytic infection. This monoclonal antibody recognises in HSV‐transformed cells polypeptides of mol. wts. 90 000, 40 000 and 32 000. Further studies show that the accumulation of these polypeptides in HSV‐transformed cells is not HSV specific but is a common feature of transformation or of cells which have been immortalised. We suggest that cellular polypeptides accumulating as a result of HSV infection may be of importance in the initiation of transformation by HSV, i.e., at the level of immortalisation of cells.

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Transformation by and Oncogenicity of Human Adenoviruses

Graham

1984

The Adenoviruses

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Adenovirus type 12-transformed rat embryo brain and rat liver epithelial cell lines: adenovirus type 12 genome content and viral protein expression

Cited by 12 publications

References 38 publications

Adenovirus 12-mediated down-regulation of the major histocompatibility complex (MHC) class I promoter: identification of a negative regulatory element responsive to Ad12 E1A

Adenovirus 12-mediated down-regulation of the major histocompatibility complex (MHC) class I promoter: identification of a negative regulatory element responsive to Ad12 E1A

Cellular proteins expressed in herpes simplex virus transformed cells also accumulate on herpes simplex virus infection.

Transformation by and Oncogenicity of Human Adenoviruses

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