Terminal cap-dependent translation enhancer. Specific interaction with RNA helicase A facilitatesTerminal cap-dependent translation enhancer. Specific

Terminal cap-dependent translation enhancer. Specific interaction with RNA helicase A facilitates
Terminal cap-dependent translation enhancer. Specific interaction with RNA helicase A facilitates polysome loading and efficient viral Deslorelin chemical information protein production. PCE is not an IRES. Readthrough of upstream AUG codons allows translation initiation of a downstream gene (i.e. vpu and env). Short upstream open reading frames present in 5′ leader RNA attenuate translation initiation at the authentic gag-pol AUG. Effect is dependent on distance from AUG. Stimulatory signal and slippery sequence present in mRNA induce ribosome pausing and a -1 reading frame change. Results in translation of gag-pol open reading frame to produce reverse transcriptase and other enzymatic proteins. Termination codon of gag open reading frame is read as glutamate. Results in translation of gag-pol open reading frame to produce reverse transcriptase and other enzymatic proteins. Scanning ribosome bypasses mRNA structural motif to reach AUG. Gag protein binds to the 5′ UTR of gag mRNA and attenuates translation efficiency. AU-rich sequences present in gag, pol and env mRNA bind cellular proteins involved in mRNA metabolism and translation. This association represses cytoplasmic expression of the mRNA. Viral regulatory protein recognizes intronic cisacting Rev response element (RRE) and counteracts repression by INS/CRS. Transactivates nuclear export, with coincide increases in mRNA stability and polysome loading that result in robust viral protein production. HTLV-1 Rex/RxRE and MMTV Rem/RmRE activity activate nuclear export and may likewise enhance translational output.Post-transcriptional control element (PCE)SNV, REV-A, HTLV-1, BLV, MPMV, FeLV, HIV-1, HFVLeaky scanningHIV-Ribosome reinitiationRSVFrameshiftingMost retrovirusesTermination codon readthroughFeLV, MLVRibosome shuntNot determinedGag-gag mRNA interactionRSV, HIV-Cis-acting repressive sequences/ inhibitory sequences (CRS/INS)HIV-RevHIV-a BLV,bovine leukemia virus; FeLV, feline leukemia virus; HFV, human foamy virus; HMSV, Harvey murine sarcoma virus; HTLV-1, human T-cell leukemia virus type 1; MLV, murine leukemia virus; MPMV, Mason-Pfizer monkey virus; REV-A, reticuloendotheliosis virus strain A; RSV, Rous sarcoma virus; SIV, simian immunodeficiency virus; SNV, spleen necrosis virus.Page 5 of(page number not for citation purposes)Retrovirology 2009, 6:http://www.retrovirology.com/content/6/1/Table 2: Retrovirus:host interactions involved in retroviral translation controlHost factor Interacts with retrovirus protein RNA Protein kinase R (PKR)Examples of interacting virusa HIV-1, HTLV-Effect on translation HIV-1 Tat reduces PKR autophosphorylation. Tat and eIF2 compete as substrates of PKR. High levels of HIV-1 TAR RNA or HTLV-1 RxRE inhibit PKR autophosphorylation. PFV Tas and HIV-1 Tat act as RNA silencing suppressors that combat the antiviral effect of small RNA pathway. Also miRNAs may be encoded by retroviruses that downregulate host antiviral defense. Binding of TRBP to HIV-1 TAR RNA results in increased HIV-1 transcription and PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26080418 translation. HIV-1 5′ UTR RNA binds 2-5OAS resulting in RNAseL activity in vitro. HIV-1 infection is associated with reduced interferon production and reduced 2-5A:RNAseL binding, allowing HIV-1 mRNA to evade cleavage by RNaseL. HTLV-1 RxRE activates 2-5OAS in vitro. RHA binds PCE PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27486068 mRNA leading to increased polysome association and efficient protein synthesis. In overexpression experiments, hyper-phosphorylated 9G8 binds constitutive transport elementcontaining reporter mRNA result.