I-Rel: a novel rel-related protein that inhibits NF-kappa B transcriptional activity
| Autor: | Chein-Hwa Chen, Timothy A. Coleman, M. Maher, Steven M. Ruben, J. F. Klement, Craig A. Rosen |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Oncogene Proteins v-rel
animal structures Transcription Genetic Protein subunit T-Lymphocytes Molecular Sequence Data Retroviridae Proteins Oncogenic Transcription Factor RelB Transcription factor complex Biology Transcription (biology) Complementary DNA Proto-Oncogene Proteins Genetics Escherichia coli Amino Acid Sequence Transcription factor Regulation of gene expression Base Sequence NF-kappa B DNA Protein-Tyrosine Kinases Blotting Northern Phosphoproteins Molecular biology Precipitin Tests Gene Expression Regulation embryonic structures Developmental Biology Transcription Factors |
| Zdroj: | Genesdevelopment. 6(5) |
| ISSN: | 0890-9369 |
| Popis: | The NF-kappa B transcription factor complex is comprised of two subunits, p50 and p65, that share significant homology to the rel oncogene. We have isolated a cDNA encoding a novel 66-kD rel-related protein, designated I-Rel. Unlike other rel-related proteins, I-Rel does not interact with DNA. I-Rel forms heterodimers with p50, however, and greatly attenuates its DNA-binding activity--an effect probably resulting from the presence of a domain inhibitory to DNA binding present within the 121 amino-terminal residues of I-Rel. In contrast, I-Rel does not associate with p65. Transfection experiments demonstrate that I-Rel suppresses NF-kappa B-induced transcription, probably through its association with p50. Expression of I-Rel mRNA is induced by mitogenic stimulation and accumulates after the appearance of p50 transcripts. Our findings suggest that p50 and I-Rel are components of a feedback pathway where expression of I-Rel may modulate indirectly the expression of genes responsive to the NF-kappa B transcription factor complex. |
| Databáze: | OpenAIRE |
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