BIOMAT Database Logo BIOMAT Database Logo

The first exon of Ad12 E1A excluding the transactivation domain mediates differential binding of COUP-TF and NF-kappa B to the MHC class I enhancer in transformed cells. 1996

D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
Department of Microbiology, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

The major histocompatibility complex class I enhancer is the target for adenovirus-12 E1A-mediated down-regulation of class I transcription. In Ad12 transformed rodent cells, the class I enhancer is down-regulated through increased binding of the repressor COUP-TF to the R2 element and decreased binding of the activator NF-kappa B (p50/p65) to the R1 element. The reduced surface levels of class I antigens contribute to the tumorigenic potential of Ad12 transformed cells by favoring their immunoescape from cytotoxic T-lymphocytes. Previous studies using transformed cells containing hybrid Ad5/Ad12 E1A (plus Ad12 E1B) genes have indicated that sequences within the first exon of the 266R Ad12 E1A gene are required for class I down-regulation and tumorigenesis. In this study we demonstrate that these same sequences, which exclude the Ad12 CR3 transactivation domain, are also required for increased COUP-TF binding to the R2 element and decreased NF-kappa B binding to the R1 element of the class I enhancer. We further show that diminished NF-kappa B binding is not due to a lack of NF-kappa B1-p50 in the nuclei of Ad12 transformed rat cells.

UI MeSH Term Description Entries
D008969 Molecular Sequence Data Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories. Sequence Data, Molecular,Molecular Sequencing Data,Data, Molecular Sequence,Data, Molecular Sequencing,Sequencing Data, Molecular
D002461 Cell Line, Transformed Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals. Transformed Cell Line,Cell Lines, Transformed,Transformed Cell Lines
D002467 Cell Nucleus Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed) Cell Nuclei,Nuclei, Cell,Nucleus, Cell
D004268 DNA-Binding Proteins Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases. DNA Helix Destabilizing Proteins,DNA-Binding Protein,Single-Stranded DNA Binding Proteins,DNA Binding Protein,DNA Single-Stranded Binding Protein,SS DNA BP,Single-Stranded DNA-Binding Protein,Binding Protein, DNA,DNA Binding Proteins,DNA Single Stranded Binding Protein,DNA-Binding Protein, Single-Stranded,Protein, DNA-Binding,Single Stranded DNA Binding Protein,Single Stranded DNA Binding Proteins
D004742 Enhancer Elements, Genetic Cis-acting DNA sequences which can increase transcription of genes. Enhancers can usually function in either orientation and at various distances from a promoter. Enhancer Elements,Enhancer Sequences,Element, Enhancer,Element, Genetic Enhancer,Elements, Enhancer,Elements, Genetic Enhancer,Enhancer Element,Enhancer Element, Genetic,Enhancer Sequence,Genetic Enhancer Element,Genetic Enhancer Elements,Sequence, Enhancer,Sequences, Enhancer
D005091 Exons The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA. Mini-Exon,Exon,Mini Exon,Mini-Exons
D005805 Genes, MHC Class I Genetic loci in the vertebrate major histocompatibility complex which encode polymorphic characteristics not related to immune responsiveness or complement activity, e.g., B loci (chicken), DLA (dog), GPLA (guinea pig), H-2 (mouse), RT-1 (rat), HLA-A, -B, and -C class I genes of man. Class I Genes,Genes, Class I,Genes, H-2 Class I,Genes, HLA Class I,MHC Class I Genes,H-2 Class I Genes,HLA Class I Genes,Class I Gene,Gene, Class I,Genes, H 2 Class I,H 2 Class I Genes
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D001483 Base Sequence The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence. DNA Sequence,Nucleotide Sequence,RNA Sequence,DNA Sequences,Base Sequences,Nucleotide Sequences,RNA Sequences,Sequence, Base,Sequence, DNA,Sequence, Nucleotide,Sequence, RNA,Sequences, Base,Sequences, DNA,Sequences, Nucleotide,Sequences, RNA
D014157 Transcription Factors Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. Transcription Factor,Factor, Transcription,Factors, Transcription

Related Publications

D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
E1A oncogene of adenovirus-12 mediates trans-repression of MHC class I transcription in Ad5/Ad12 somatic hybrid transformed cells.
September 1994, Virology,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
Association of histone deacetylase with COUP-TF in tumorigenic Ad12-transformed cells and its potential role in shut-off of MHC class I transcription.
March 2000, Virology,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
Negative regulation by the R2 element of the MHC class I enhancer in adenovirus-12 transformed cells correlates with high levels of COUP-TF binding.
August 1994, Oncogene,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
I kappa B/MAD-3 masks the nuclear localization signal of NF-kappa B p65 and requires the transactivation domain to inhibit NF-kappa B p65 DNA binding.
December 1992, Molecular biology of the cell,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
Reduced binding activity of transcription factor NF-kappa B accounts for MHC class I repression in adenovirus type 12 E 1-transformed cells.
November 1992, Cellular immunology,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
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.
December 1991, The EMBO journal,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
NF-kappa B p65 transactivation domain is involved in the NF-kappa B-inducing kinase pathway.
February 2003, Biochemical and biophysical research communications,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
E1A is the component of the MHC class I enhancer complex that mediates HDAC chromatin repression in adenovirus-12 tumorigenic cells.
September 2006, Virology,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
Differential expression of LFA-3, Fas and MHC Class I on Ad5- and Ad12-transformed human cells and their susceptibility to lymphokine-activated killer (LAK) cells.
August 2005, Virology,
D B Kushner, and D S Pereira, and X Liu, and F L Graham, and R P Ricciardi
TNF stimulates expression of mouse MHC class I genes by inducing an NF kappa B-like enhancer binding activity which displaces constitutive factors.
December 1989, The EMBO journal,
Copied contents to your clipboard!