Transcription Intermediary Factor 1gamma Decreases Protein Expression of the Transcriptional Cofactor, LIM-Domain-Binding 1
- Howard, P.W., Ransom, D.G., and Maurer, R.A.
- Biochemical and Biophysical Research Communications 396(3): 674-678 (Journal)
- Registered Authors
- Ransom, David G.
- Ubiquitin ligase, LIM-homeodomain transcription factor, Proteasome
- MeSH Terms
- CHO Cells
- Cell Line
- DNA-Binding Proteins/biosynthesis*
- DNA-Binding Proteins/genetics
- Gene Expression Regulation
- Gene Knockdown Techniques
- LIM Domain Proteins
- Promoter Regions, Genetic
- Transcription Factors/biosynthesis*
- Transcription Factors/genetics
- Transcription Factors/metabolism*
- 20447379 Full text @ Biochem. Biophys. Res. Commun.
Howard, P.W., Ransom, D.G., and Maurer, R.A. (2010) Transcription Intermediary Factor 1gamma Decreases Protein Expression of the Transcriptional Cofactor, LIM-Domain-Binding 1. Biochemical and Biophysical Research Communications. 396(3):674-678.
LIM-domain-binding 1 (LDB1) is a cofactor that participates in formation of regulatory complexes involving transcription factors containing LIM domains as well as other factors. We have examined the ability of transcriptional Intermediary factor 1gamma (TIF1gamma) to decrease LDB1 expression. An expression vector for TIF1gamma was found to decrease expression of LDB1. A mutation which disrupts the ubiquitin ligase activity of TIF1gamma was found to block the ability of TIF1gamma to decrease LDB1 expression. Proteasome inhibitors were also able to block TIF1gamma effects on LDB1. Immunoprecipitation studies provided evidence that LDB1 interacts with TIF1gamma in intact cells. Knockdown of TIF1gamma in zebrafish embryos led to increased expression of LDB1 providing evidence for a physiological role of TIF1gamma in regulating LDB1 expression. Reporter gene assays demonstrated that TIF1gamma can alter the activity of LIM-homeodomain transcription factor-responsive promoters. These studies are consistent with a model in which TIF1gamma acts to ubiquitinate LDB1 leading to degradation of LDB1 and changes in transcription of LDB1-dependent promoters.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes