Role for N-CoR and histone deacetylase in Sin3-mediated transcriptional repression

被引：732

作者：

Alland, L

Muhle, R

Hou, H

Potes, J

Chin, L

SchreiberAgus, N

DePinho, RA

机构：

[1] ALBERT EINSTEIN COLL MED, DEPT MICROBIOL & IMMUNOL, NEW YORK, NY 10461 USA

[2] ALBERT EINSTEIN COLL MED, DEPT PEDIAT, NEW YORK, NY 10461 USA

[3] ALBERT EINSTEIN COLL MED, DIV DERMATOL, NEW YORK, NY 10461 USA

来源：

NATURE | 1997年 / 387卷 / 6628期

关键词：

D O I：

10.1038/387049a0

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Normal mammalian growth and development ave highly dependent on the regulation of the expression and activity of the Myo family of transcription factors. Mxi1-mediated inhibition of Myc activities requires interaction with mammalian Sin3A or Sin3B proteins, which have been purported to act as scaffolds for additional co-repressor factors. The identification of two such Sin3-associated factors, the nuclear receptor co-repressor (N-CoR) and histone deacetylase (HD1), provides a basis for Mxi1/Sin3-induced transcriptional repression and tumour suppression.

引用

页码：49 / 55

页数：7

共 50 条

[1]

Ayer DE, 1996, MOL CELL BIOL, V16, P5772

[2] MAD-MAX TRANSCRIPTIONAL REPRESSION IS MEDIATED BY TERNARY COMPLEX-FORMATION WITH MAMMALIAN HOMOLOGS OF YEAST REPRESSOR SIN3 [J].