Kim Y K, Hahm B, Jang S K
NRL, Department of Life Science, Division of Molecular and Life Sciences, Pohang University of Science and Technology, San31, Pohang, Hyoja-Dong, 790-784, Korea.
J Mol Biol. 2000 Nov 24;304(2):119-33. doi: 10.1006/jmbi.2000.4179.
Translation initiation of human Bip mRNA is directed by an internal ribosomal entry site (IRES) located in the 5' non-translated region. No trans-acting factor possibly involved in this process has as of yet been identified. For the encephalomyocarditis virus and other picornaviruses, polypyrimidine tract-binding protein (PTB) has been found to enhance the translation through IRES elements, probably by interaction with the IRES structure. Here, we report that PTB specifically binds to the central region (nt 50-117) of the Bip 5' non-translated region. Addition of purified PTB to rabbit reticulocyte lysate and overexpression of PTB in Cos-7 cells selectively inhibited Bip IRES-dependent translation. On the other hand, depletion of endogenous PTB or addition of an RNA interacting with PTB enhanced the translational initiation directed by Bip IRES. These suggest that PTB can either enhance or inhibit IRES-dependent translation depending on mRNAs.
人Bip mRNA的翻译起始由位于5'非翻译区的一个内部核糖体进入位点（IRES）指导。截至目前，尚未鉴定出可能参与此过程的反式作用因子。对于脑心肌炎病毒和其他微小核糖核酸病毒，已发现多嘧啶序列结合蛋白（PTB）可通过IRES元件增强翻译，可能是通过与IRES结构相互作用。在此，我们报告PTB特异性结合Bip 5'非翻译区的中央区域（核苷酸50 - 117）。向兔网织红细胞裂解物中添加纯化的PTB以及在Cos - 7细胞中过表达PTB选择性抑制了Bip IRES依赖性翻译。另一方面，内源性PTB的缺失或添加与PTB相互作用的RNA增强了由Bip IRES指导的翻译起始。这些结果表明，PTB可根据mRNA增强或抑制IRES依赖性翻译。
