Blinder D, Coschigano P W, Magasanik B
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.
J Bacteriol. 1996 Aug;178(15):4734-6. doi: 10.1128/jb.178.15.4734-4736.1996.
We used cells carrying plasmids causing the overproduction of Gln3p, Ure2p, or both of these proteins to elucidate the ability of Ure2p to prevent the activation of gene expression by Gln3p in cells growing in a glutamine-containing medium. Our results indicate that Ure2p probably does not interfere with the binding of the GATA factor Gln3p to GATAAG sites but acts directly on Gln3p to block its ability to activate transcription.
我们使用携带能导致Gln3p、Ure2p或这两种蛋白质过量产生的质粒的细胞,来阐明在含谷氨酰胺培养基中生长的细胞里,Ure2p阻止Gln3p激活基因表达的能力。我们的结果表明,Ure2p可能不会干扰GATA因子Gln3p与GATAAG位点的结合,而是直接作用于Gln3p以阻断其激活转录的能力。