Literature DB >> 2800342

Nuclear proteins binding to an enhancer element of the major histocompatibility class I promoter: differences between highly oncogenic and nononcogenic adenovirus-transformed rat cells.

A M Ackrill1, G E Blair.   

Abstract

Two major DNA-binding activities specific for the major histocompatibility (MHC) class I regulatory element (CRE) were detected in adenovirus (Ad)-transformed cells. One activity, term CRE1, had similar binding properties to a previously described positive-acting transcription factor specific for MHC class I genes termed H2TF1. The other activity, termed CRE2, bound to a region on the CRE separate from CRE1, and was present in Ad12, but not in Ad5-transformed cells. A CRE2-like activity was also present in non-adenovirus-transformed mouse L929 cells, indicating that CRE2 may be a cellular, rather than a viral, factor. The CRE2 activity did not correspond to any previously described transcription factor with a potential binding site in the CRE.

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Year:  1989        PMID: 2800342     DOI: 10.1016/0042-6822(89)90207-9

Source DB:  PubMed          Journal:  Virology        ISSN: 0042-6822            Impact factor:   3.616


  12 in total

1.  Impairment of MHC class I transcription in a mutant bovine B cell line.

Authors:  J S Harms; G A Splitter
Journal:  Immunogenetics       Date:  1992       Impact factor: 2.846

Review 2.  Expression and interactions of human adenovirus oncoproteins.

Authors:  P A Boulanger; G E Blair
Journal:  Biochem J       Date:  1991-04-15       Impact factor: 3.857

3.  In adenovirus type 12 tumorigenic cells, major histocompatibility complex class I transcription shutoff is overcome by induction of NF-kappaB and relief of COUP-TFII repression.

Authors:  Shihe Hou; Hancheng Guan; Robert P Ricciardi
Journal:  J Virol       Date:  2002-04       Impact factor: 5.103

4.  A multiprotein complex consisting of the cellular coactivator p300, AP-1/ATF, as well as NF-kappaB is responsible for the activation of the mouse major histocompatibility class I (H-2K(b)) enhancer A.

Authors:  D Brockmann; B M Pützer; K S Lipinski; U Schmücker; H Esche
Journal:  Gene Expr       Date:  1999

5.  Reduced phosphorylation of p50 is responsible for diminished NF-kappaB binding to the major histocompatibility complex class I enhancer in adenovirus type 12-transformed cells.

Authors:  D B Kushner; R P Ricciardi
Journal:  Mol Cell Biol       Date:  1999-03       Impact factor: 4.272

6.  Down-regulation of the major histocompatibility complex class I enhancer in adenovirus type 12-transformed cells is accompanied by an increase in factor binding.

Authors:  R Ge; A Kralli; R Weinmann; R P Ricciardi
Journal:  J Virol       Date:  1992-12       Impact factor: 5.103

7.  Negative regulation of the major histocompatibility complex class I enhancer in adenovirus type 12-transformed cells via a retinoic acid response element.

Authors:  A Kralli; R Ge; U Graeven; R P Ricciardi; R Weinmann
Journal:  J Virol       Date:  1992-12       Impact factor: 5.103

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

Authors:  J L Proffitt; E Sharma; G E Blair
Journal:  Nucleic Acids Res       Date:  1994-11-11       Impact factor: 16.971

9.  Driving adenovirus type 12-transformed BALB/c mouse cells to express high levels of class I major histocompatibility complex proteins enhances, rather than abrogates, their tumorigenicity.

Authors:  S Soddu; A M Lewis
Journal:  J Virol       Date:  1992-05       Impact factor: 5.103

10.  Changes in NF-kappa B and ISGF3 DNA binding activities are responsible for differences in MHC and beta-IFN gene expression in Ad5- versus Ad12-transformed cells.

Authors:  U Nielsch; S G Zimmer; L E Babiss
Journal:  EMBO J       Date:  1991-12       Impact factor: 11.598

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