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Cited by 19 publications
(14 citation statements)
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References 37 publications
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“…2B). Many RNA viruses, including encephalomyocarditis virus (EMCV), poliovirus, cricket paralysis virus (CrPV), VSV, Sindbis virus (SINV), Dengue virus (DENV), and reovirus (Gingras et al 1996;Connor and Lyles 2002;Villas-Boas et al 2009;Garrey et al 2010;Mohankumar et al 2011), as well as small DNA viruses such as SV40 (Yu et al 2005), induce the accumulation of hypophosphorylated 4E-BP1, which sequesters the cap-binding subunit eIF4E and prevents eIF4F assembly (Hinnebusch and Lorsch 2012;Roux and Topisirovic 2012). In the case of VSV, this requires the viral M protein, which suppresses Akt-signaling to prevent mTORC1-mediated inactivation of 4E-BP1 (Dunn and Connor 2011).…”
Section: Indirect Effects On Cellular Translation Factorsmentioning
confidence: 99%
“…2B). Many RNA viruses, including encephalomyocarditis virus (EMCV), poliovirus, cricket paralysis virus (CrPV), VSV, Sindbis virus (SINV), Dengue virus (DENV), and reovirus (Gingras et al 1996;Connor and Lyles 2002;Villas-Boas et al 2009;Garrey et al 2010;Mohankumar et al 2011), as well as small DNA viruses such as SV40 (Yu et al 2005), induce the accumulation of hypophosphorylated 4E-BP1, which sequesters the cap-binding subunit eIF4E and prevents eIF4F assembly (Hinnebusch and Lorsch 2012;Roux and Topisirovic 2012). In the case of VSV, this requires the viral M protein, which suppresses Akt-signaling to prevent mTORC1-mediated inactivation of 4E-BP1 (Dunn and Connor 2011).…”
Section: Indirect Effects On Cellular Translation Factorsmentioning
confidence: 99%
“…It is not known how flavivirus genome RNA translation efficiently competes with cell mRNA translation. Dephosphorylation of p70S6K and 4E-BP1 in infected cells was detected starting at 24 hours after infection (Villas-Boas, Conceicao et al 2009) and cap-independent translation of genome RNA was observed when eIF4E levels were low (Edgil, Polacek et al 2006) suggesting that flavivirus RNA translation may switch to an as yet unknown cap-independent mechanism at later times of infection. Both the 3′ and 5′ NCRs of the flavivirus genome were shown to be required for cap-independent translation.…”
Section: Cell Protein Involvement In Viral Rna Translationmentioning
confidence: 99%
“…How flavivirus genome translation efficiently competes with the cell mRNAs, since both have a 5' cap, is not known. The observed upregulation of cap-dependent translation factors prior to 24 h after infection but dephosphorylation of p70S6K and 4E-BP1 at 24 and 48 h [211], as well as the observation of cap-dependent translation of a flavivirus genome when eIF4E was abundant but cap-independent translation when eIF4E levels were low [212], suggests the possibility that the viral RNA may switch to a cap-independent translation mechanism at later times of infection. Both the 3' and 5' UTRs of the flavivirus genome were reported to be required for cap-independent translation.…”
Section: Viral Rna Translation and Replicationmentioning
confidence: 99%