FdvOgp1

Summary

Gene Symbol: FdvOgp1
Description: pol protein
Species: Foot-and-mouth disease virus - type O

Top Publications

  1. Wang D, Fang L, Li K, Zhong H, Fan J, Ouyang C, et al. Foot-and-mouth disease virus 3C protease cleaves NEMO to impair innate immune signaling. J Virol. 2012;86:9311-22 pubmed publisher
    ..Collectively, our data identify NEMO as a substrate for FMDV 3C(pro) and reveal a novel mechanism evolved by a picornavirus to counteract innate immune signaling...
  2. Gladue D, O Donnell V, Baker Branstetter R, Holinka L, Pacheco J, Fernandez Sainz I, et al. Foot-and-mouth disease virus nonstructural protein 2C interacts with Beclin1, modulating virus replication. J Virol. 2012;86:12080-90 pubmed publisher
    ..These results suggest that interaction between FMDV 2C and host protein Beclin1 could be essential for virus replication...
  3. Armer H, Moffat K, Wileman T, Belsham G, Jackson T, Duprex W, et al. Foot-and-mouth disease virus, but not bovine enterovirus, targets the host cell cytoskeleton via the nonstructural protein 3Cpro. J Virol. 2008;82:10556-66 pubmed publisher
    ..In contrast, infection of cells with another picornavirus, bovine enterovirus, did not affect gamma-tubulin distribution, and the microtubule network remained relatively unaffected...
  4. Borca M, Pacheco J, Holinka L, Carrillo C, Hartwig E, Garriga D, et al. Role of arginine-56 within the structural protein VP3 of foot-and-mouth disease virus (FMDV) O1 Campos in virus virulence. Virology. 2012;422:37-45 pubmed publisher
    ..O1Ca-VP3-56H was thermo stable and induced typical clinical signs of FMD, whereas O1Ca-VP3-56R presented a ts phenotype and was nonpathogenic unless VP3 position 56 reverted in vivo to either H or cysteine (C)...
  5. Zhu Z, Wang G, Yang F, Cao W, Mao R, Du X, et al. Foot-and-Mouth Disease Virus Viroporin 2B Antagonizes RIG-I-Mediated Antiviral Effects by Inhibition of Its Protein Expression. J Virol. 2016;90:11106-11121 pubmed
    ..This study provides new insight into the immune evasion mediated by FMDV and identifies 2B as an antagonistic factor for FMDV to evade the antiviral response. ..
  6. Gladue D, O Donnell V, Baker Branstetter R, Holinka L, Pacheco J, Fernandez Sainz I, et al. Foot-and-mouth disease virus modulates cellular vimentin for virus survival. J Virol. 2013;87:6794-803 pubmed publisher
    ..Using reverse genetics, we identified 2C residues that are necessary for virus growth, suggesting that the interaction between FMDV 2C and cellular vimentin is essential for virus replication. ..
  7. Li D, Wei J, Yang F, Liu H, Zhu Z, Cao W, et al. Foot-and-mouth disease virus structural protein VP3 degrades Janus kinase 1 to inhibit IFN-γ signal transduction pathways. Cell Cycle. 2016;15:850-60 pubmed publisher
    ..Taken together, the results reveal a novel mechanism used by which FMDV VP3 counteracts the type II IFN signaling pathways. ..
  8. Jiang S, Bai X, Li P, Zhang M, Bao H, Sun P, et al. Influence of Foot-and-Mouth Disease Virus O/CHN/Mya98/33-P Strain Leader Protein on Viral Replication and Host Innate Immunity. Viral Immunol. 2015;28:360-6 pubmed publisher
    ..Additionally, the Lb of FMDV O/CHN/Mya98/33-P must be involve in increasing its ability to inhibit host innate immune response, and the distinctive amino acids G56 and/or R118 of FMDV leader protein may play essential roles in it. ..
  9. Li X, Wang J, Liu J, Li Z, Wang Y, Xue Y, et al. Engagement of soluble resistance-related calcium binding protein (sorcin) with foot-and-mouth disease virus (FMDV) VP1 inhibits type I interferon response in cells. Vet Microbiol. 2013;166:35-46 pubmed publisher
    ..Thus, VP1-induced suppression of type I interferon is mediated by interacting with sorcin, a protein that appears to regulate cell response to viral infections. ..

More Information

Publications17

  1. Fan X, Han S, Yan D, Gao Y, Wei Y, Liu X, et al. Foot-and-mouth disease virus infection suppresses autophagy and NF-кB antiviral responses via degradation of ATG5-ATG12 by 3Cpro. Cell Death Dis. 2017;8:e2561 pubmed publisher
    ..FMDV has evolved mechanisms to counteract the antiviral function of ATG5-ATG12, via degradation of them by viral protein 3Cpro. ..
  2. Rai D, Lawrence P, Kloc A, Schafer E, Rieder E. Analysis of the interaction between host factor Sam68 and viral elements during foot-and-mouth disease virus infections. Virol J. 2015;12:224 pubmed publisher
    ..These results support the importance of Sam68 as a host factor co-opted by FMDV during infection and demonstrate that Sam68 interact with both, FMDV RNA motifs in the IRES and viral non-structural proteins 3C(pro) and 3D(pol). ..
  3. Zhu Z, Yang F, Zhang K, Cao W, Jin Y, Wang G, et al. Comparative Proteomic Analysis of Wild-Type and SAP Domain Mutant Foot-and-Mouth Disease Virus-Infected Porcine Cells Identifies the Ubiquitin-Activating Enzyme UBE1 Required for Virus Replication. J Proteome Res. 2015;14:4194-206 pubmed publisher
    ..Overexpression of UBE1 enhanced the replication of FMDV, and knockdown of UBE1 decreased FMDV replication. This shows that FMDV manipulates UBE1 for increased viral replication, and the SAP domain was involved in this process. ..
  4. Chamberlain K, Fowler V, Barnett P, Gold S, Wadsworth J, Knowles N, et al. Identification of a novel cell culture adaptation site on the capsid of foot-and-mouth disease virus. J Gen Virol. 2015;96:2684-92 pubmed publisher
    ..These observations add to the evidence for multiple cell attachment mechanisms for FMDV and may be useful for vaccine manufacture when cell culture adaptation proves difficult. ..
  5. Zheng W, Li X, Wang J, Li X, Cao H, Wang Y, et al. A critical role of interferon-induced protein IFP35 in the type I interferon response in cells induced by foot-and-mouth disease virus (FMDV) protein 2C. Arch Virol. 2014;159:2925-35 pubmed publisher
    ..These findings may help to further understand cell responses to FMDV infection. ..
  6. Beard C, Mason P. Genetic determinants of altered virulence of Taiwanese foot-and-mouth disease virus. J Virol. 2000;74:987-91 pubmed
    ..These studies have shown that an altered nonstructural protein, 3A, is a primary determinant of restricted growth on bovine cells in vitro and significantly contributes to bovine attenuation of OTai in vivo...
  7. Polacek C, Gullberg M, Li J, Belsham G. Low levels of foot-and-mouth disease virus 3C protease expression are required to achieve optimal capsid protein expression and processing in mammalian cells. J Gen Virol. 2013;94:1249-58 pubmed publisher
  8. Arias A, Agudo R, Ferrer Orta C, P rez Luque R, Airaksinen A, Brocchi E, et al. Mutant viral polymerase in the transition of virus to error catastrophe identifies a critical site for RNA binding. J Mol Biol. 2005;353:1021-32 pubmed publisher
    ..In addition to identifying an amino acid residue that is critical for the binding of polymerase to RNA, the results document the presence of defective genomes in the transition of virus to error catastrophe...