Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.3.14 (ATP synthase)
 7,042 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The beta-subunit of the mitochondrial H+-ATP synthase (beta-F1-ATPase) catalyzes the rate-limiting step of ATP formation in eukaryotic cells. Here, we examined the post-transcriptional regulation of human beta-F1-ATPase mediated by the 3'-untranslated region of the mRNA (beta-3'-UTR). Biochemical analysis revealed that the adenosine/uridine (AU)-rich element-binding proteins TIA-1 (T-cell intracellular antigen-1), TIAR (TIA-1-related protein), and HuR (Hu antigen R) interact with the beta-F1-ATPase mRNA through an AU-rich sequence located to the 3'-UTR. Mouse embryonic fibroblasts (MEFs) knocked-out for TIA-1 or RNA interference (RNAi)-mediated knockdown of endogenous TIA-1, TIAR, or HuR in HeLa cells resulted in a decrease in beta-F1-ATPase protein expression. The expression of GFP from a chimeric reporter containing human beta-3'-UTR was also abolished in HeLa cells depleted of TIA-1, TIAR, or HuR. MEFs knocked-in for TIA-1 or the overexpression of RNAi-resistant TIA-1, TIAR, or HuR proteins in the RNAi-treated HeLa cells significantly restored the levels of the expression of both endogenous mouse beta-F1-ATPase protein or recombinant GFP.
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PMID:Control of the ATP synthase beta subunit expression by RNA-binding proteins TIA-1, TIAR, and HuR. 1689 Jan 99

We have recently reported that RNA-binding proteins TIA-1 (T-cell intracellular antigen-1), TIAR (TIA-1 related protein), and HuR (Hu antigen R) modulate the expression of the ATP synthase beta-subunit mRNA (beta-F1-ATPase mRNA) [J.M. Izquierdo, Control of the ATP synthase beta subunit expression by RNA-binding proteins TIA-1, TIAR, and HuR, Biochem. Biophys. Res. Commun. 348 (2006) 703-711]. Here we found that PTB (Polypyrimidine Tract-Binding Protein) is a novel member of the ribonucleoprotein complex that interacts with the beta-F1-ATPase mRNA through an adenosine/uridine (AU)-rich element located to the beta-F1-ATPase 3'-untranslated region (beta-3'-UTR). Co-expression of GFP from a reporter mRNA quimera containing human beta-3'-UTR and recombinant PTB in HeLa cells increased the amount of GFP protein. Interestingly, this effect is not due to increased steady-state levels of GFP-beta-3'-UTR mRNA. Taken together, these results suggest that PTB regulates post-transcriptional expression of the beta-F1-ATPase mRNA at the translational level.
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PMID:The RNA-binding protein PTB exerts translational control on 3'-untranslated region of the mRNA for the ATP synthase beta-subunit. 1746 48