Mammalian elongin A is not essential for cell viability but is required for proper cell cycle progression with limited alteration of gene expression

被引:15
|
作者
Yamazaki, K
Aso, T
Ohnishi, Y
Ohno, M
Tamura, K
Shuin, T
Kitajima, S
Nakabeppu, Y
机构
[1] Kochi Med Sch, Fac Med, Dept Chem, Nanko Ku, Kochi 7838505, Japan
[2] Kochi Med Sch, Fac Med, Dept Urol, Nanko Ku, Kochi 7838505, Japan
[3] Japan Sci & Technol Corp, CREST, Higashi Ku, Fukuoka 8128582, Japan
[4] Kyushu Univ, Med Inst Bioregulat, Higashi Ku, Fukuoka 8128582, Japan
[5] Japan Sci & Technol, CREST, Higashi Ku, Fukuoka 8128582, Japan
[6] Tokyo Med & Dent Univ, Dept Biochem Genet, Inst Med Res, Bunkyo Ku, Tokyo 1138510, Japan
关键词
D O I
10.1074/jbc.C300047200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Elongin A is a transcription elongation factor that increases the overall rate of mRNA chain elongation by RNA polymerase II To investigate the function of Elongin A in vivo, the two alleles of the Elongin A gene have been disrupted by homologous recombination in murine embryonic stem (ES) cells. The Elongin A-deficient ES cells are viable, but show a slow growth phenotype because they undergo a delayed mitosis. The cDNA microarray and RNase protection assay using the wildtype and Elongin A-deficient ES cells indicate that the expression of only a small subset of genes is affected in the mutant cells. Taken together, our results suggest that Elongin A regulates transcription of a subset but not all of genes and reveal a linkage between Elongin A function and cell cycle progression.
引用
收藏
页码:13585 / 13589
页数:5
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