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10.1134/S0006297921090042 http://scihub22266oqcxt.onion/10.1134/S0006297921090042 34565312!8436584!34565312     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochemistry+(Mosc) 2021 ; 86 (9): 1060-1094 Nephropedia Template TP {{tp|p=34565312|t=2021. Non-Canonical Translation Initiation Mechanisms Employed by Eukaryotic Viral mRNAs |pdf=|usr=}}{{34565312}} gab.com Text Non-Canonical Translation Initiation Mechanisms Employed by Eukaryotic Viral mRNAs JO: Biochemistry (Mosc) http://www.kidney.de/pget.php?&tw=1&pmid=34565312 #FOAvip Viruses exploit the translation machinery of an infected cell to synthesize their proteins. Therefore, viral mRNAs have to compete for ribosomes and translation factors with cellular mRNAs. To succeed, eukaryotic viruses adopt multiple strategies. One is to circumvent the need for m(7)G-cap through alternative instruments for ribosome recruitment. These include internal ribosome entry sites (IRESs), which make translation independent of the free 5' end, or cap-independent translational enhancers (CITEs), which promote initiation at the uncapped 5' end, even if located in 3' untranslated regions (3' UTRs). Even if a virus uses the canonical cap-dependent ribosome recruitment, it can still perturb conventional ribosomal scanning and start codon selection. The pressure for genome compression often gives rise to internal and overlapping open reading frames. Their translation is initiated through specific mechanisms, such as leaky scanning, 43S sliding, shunting, or coupled termination-reinitiation. Deviations from the canonical initiation reduce the dependence of viral mRNAs on translation initiation factors, thereby providing resistance to antiviral mechanisms and cellular stress responses. Moreover, viruses can gain advantage in a competition for the translational machinery by inactivating individual translational factors and/or replacing them with viral counterparts. Certain viruses even create specialized intracellular "translation factories", which spatially isolate the sites of their protein synthesis from cellular antiviral systems, and increase availability of translational components. However, these virus-specific mechanisms may become the Achilles' heel of a viral life cycle. Thus, better understanding of the unconventional mechanisms of viral mRNA translation initiation provides valuable insight for developing new approaches to antiviral therapy. Twit Text FOAVip Non-Canonical Translation Initiation Mechanisms Employed by Eukaryotic Viral mRNAs ????Biochemistry (Mosc) http://www.kidney.de/pget.php?&tw=1&pmid=34565312 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34565312 #FOAvip English Wikipedia <ref>{{Cite pmid|34565312}}</ref> Non-Canonical Translation Initiation Mechanisms Employed by Eukaryotic Viral mRNAs #MMPMID34565312 Sorokin II; Vassilenko KS; Terenin IM; Kalinina NO; Agol VI; Dmitriev SE Biochemistry (Mosc) 2021[Sep]; 86 (9): 1060-1094 PMID34565312show ga Viruses exploit the translation machinery of an infected cell to synthesize their proteins. Therefore, viral mRNAs have to compete for ribosomes and translation factors with cellular mRNAs. To succeed, eukaryotic viruses adopt multiple strategies. One is to circumvent the need for m(7)G-cap through alternative instruments for ribosome recruitment. These include internal ribosome entry sites (IRESs), which make translation independent of the free 5' end, or cap-independent translational enhancers (CITEs), which promote initiation at the uncapped 5' end, even if located in 3' untranslated regions (3' UTRs). Even if a virus uses the canonical cap-dependent ribosome recruitment, it can still perturb conventional ribosomal scanning and start codon selection. The pressure for genome compression often gives rise to internal and overlapping open reading frames. Their translation is initiated through specific mechanisms, such as leaky scanning, 43S sliding, shunting, or coupled termination-reinitiation. Deviations from the canonical initiation reduce the dependence of viral mRNAs on translation initiation factors, thereby providing resistance to antiviral mechanisms and cellular stress responses. Moreover, viruses can gain advantage in a competition for the translational machinery by inactivating individual translational factors and/or replacing them with viral counterparts. Certain viruses even create specialized intracellular "translation factories", which spatially isolate the sites of their protein synthesis from cellular antiviral systems, and increase availability of translational components. However, these virus-specific mechanisms may become the Achilles' heel of a viral life cycle. Thus, better understanding of the unconventional mechanisms of viral mRNA translation initiation provides valuable insight for developing new approaches to antiviral therapy. |Animals[MESH] |Eukaryotic Cells/physiology/*virology[MESH] |Humans[MESH] |Internal Ribosome Entry Sites/physiology[MESH] |Peptide Chain Initiation, Translational/*physiology[MESH] |RNA, Circular/genetics[MESH] |RNA, Messenger/*genetics/*metabolism[MESH] |RNA, Viral/*genetics/*metabolism[MESH]Non-Canonical Translation Initiation Mechanisms Employed by Eukaryotic(epmc).pdf DeepDyve Pubget Overpricing