Abstract:
:PML-RARalpha is a chimeric transcription factor tightly associated with acute promyelocytic leukemia. PML-RARalpha plays an important role in the aberrant transcription repression on the target genes of wild-type retinoic acid receptors. Here, we demonstrated that HDAC3, one component of the N-CoR transcription repressor complex, is a key regulator of the transcription repression by PML-RARalphain vivo. Using immunoprecipitation, we demonstrated that PML-RARalpha interacts with N-CoR/HDAC3 in vivo without ligand. Next, using chromatin immunoprecipitation (ChIP) assay, this N-CoR/HDAC3 co-repressor complex was recruited to the endogenous target promoters (RARbeta and CYP26) through PML-RARalpha. The neighboring histones were de-acetylated and gene expression was repressed. When HDAC3 protein was knocked down by RNA interference in PML-RARalpha-expressing cells, the endogenous target genes were significantly activated, which was also confirmed by promoter-luciferase reporter assay. These results provide evidence to show that the N-CoR/HDAC3 co-repressor complex is involved in the aberrant transcription regulation in PML-RARalpha-expressing cells.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Atsumi A,Tomita A,Kiyoi H,Naoe Tdoi
10.1016/j.bbrc.2006.05.047subject
Has Abstractpub_date
2006-07-14 00:00:00pages
1471-80issue
4eissn
0006-291Xissn
1090-2104pii
S0006-291X(06)01090-4journal_volume
345pub_type
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