Co-regulated expression of junB and MHC class I genes in adenovirus-transformed cells

Oncogene. 1991 Jun;6(6):911-6.

Abstract

The expression of the junB gene parallels the expression of the MHC class I genes in Adenovirus (Ad) transformed cells. In Ad12E1-transformed primary BRK cells both genes are transcriptionally repressed only when the 13S product of Ad12E1A is present. This indicates that repression of MHC class I and junB genes is a function of conserved region 3 (CR3) of the Ad12E1A protein. In Ad5-transformed BRK cells expression of these genes is unchanged. In established NRK cells, however, introduction of Ad12E1A does not cause repression of the MHC class I and junB genes, but in these cells Ad5E1A increases the expression of both MHC class I and junB. Using mutant Ad5E1A genes, it is shown that this activation is mediated by CR1. Introduction of a functional junB gene under the control of a heterologous promoter in Ad12E1-transformed BRK cells causes no increase in MHC class I expression. This demonstrates that the down-regulation of junB is not directly responsible for class I repression, but rather that both genes are coregulated by the Ad12E1 region.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviruses, Human / genetics*
  • Adenoviruses, Human / metabolism
  • Adenoviruses, Human / physiology
  • Animals
  • Base Sequence
  • Cell Line, Transformed
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Down-Regulation / genetics
  • Gene Expression Regulation, Viral*
  • Genes, MHC Class I / physiology*
  • Histocompatibility Antigens Class I / genetics*
  • Histocompatibility Antigens Class I / metabolism
  • Humans
  • Molecular Sequence Data
  • Promoter Regions, Genetic / genetics
  • Proto-Oncogene Proteins c-jun
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism
  • Transcription, Genetic / genetics

Substances

  • DNA-Binding Proteins
  • Histocompatibility Antigens Class I
  • Proto-Oncogene Proteins c-jun
  • Transcription Factors