Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/60359
標題: Transcriptional repression activity of PAX3 is modulated by competition between corepressor KAP1 and heterochromatin protein 1
作者: Hsieh, M.J.
楊文明
Yao, Y.L.
Lai, I.L.
Yang, W.M.
關鍵字: Pax3
HP1
KAP1
heterochromatin
subcellular localization
competition
tumor alveolar rhabdomyosarcoma
waardenburg syndrome type-1
hp1 chromo
domain
cell-differentiation
histone methylation
gene
translocation
deacetylases
activation
components
期刊/報告no:: Biochemical and Biophysical Research Communications, Volume 349, Issue 2, Page(s) 573-581.
摘要: Pax3 is a transcription factor crucial for normal development and tumorigenesis. Pax3 has been known to cause Waardenburg syndrome and pediatric alveolar rhabdomyosarcoma, but how Pax3 regulates transcription is not clear. Here, we report that Pax3 represses transcription and selectively interacts with heterochromatin protein 1 (HP1) and KAP1. KAP1 functions as a transcriptional corepressor by recruiting HP1 to facilitate the formation of a closed chromatin through histone deacetylation and methylation. We found that KAP1 is a corepressor for Pax3 by augmenting the repressional activity of Pax3. Unexpectedly, HP1 gamma diminishes the repressional activity of Pax3. On target promoters, KAP1 and HP1 gamma compete for binding with Pax3 on the N-terminal paired domain, and the C-terminal domain of Pax3 governs the subcellular localization of Pax3. Taken together, our results indicate that Pax3 represses transcription through a novel mechanism involving competition between corepressor KAP1 and the heterochromatin-binding protein HP1 gamma. (c) 2006 Elsevier Inc. All rights reserved.
URI: http://hdl.handle.net/11455/60359
ISSN: 0006-291X
文章連結: http://dx.doi.org/10.1016/j.bbrc.2006.08.064
Appears in Collections:分子生物學研究所

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