Viral and cellular kinases play a central role in VZV pathogenesis and are targets for antiviral kinase inhibitors

• Autorzy: Moffat J F , Taylor S.L. , Leisenfelder S.
• Języki publikacji: EN

Słowa kluczowe

EN

pathogenesis; antiviral kinase inhibitor; cell; virus; interaction; cellular protein; viral kinase; herpesvirus; cellular kinase

• Wydawca: -
• Czasopismo: Cellular and Molecular Biology Letters
• Rocznik: 2003
• Tom: 08
• Numer: 2A
• Opis fizyczny: p.537-540

Twórcy

autor

Moffat J F

• SUNY Upstate Medical University, Syracuse, NY 13210, USA

autor

Taylor S.L.

autor

Leisenfelder S.

Bibliografia

• 1.Kenyon, T.K., Cohen, J.I. and Grose, C. Phosphorylation by the varicella-zoster virus ORF47 protein serine kinase determines whether endocytosed viral gE traffics to the trans- Golgi network or recycles to the cell membrane. J. Virol. 76 (2002) 10980-10993.
• 2.Kenyon, T.K., Lynch, J., Hay, J., Ruyechan, W. and Grose, C. Varicella-zoster virus ORF47 protein serine kinase: Characterization of a cloned, biologically active phosphotransferase and two viral substrates, ORF62 and ORF63. J. Virol. 75 (2001) 8854-8858.
• 3.Moffat, J.F., Zerboni, L., Sommer, M.H., Heineman, T.C., Cohen, J.I., Kaneshima, H. and Arvin, A.M. The ORF47 and ORF66 putative protein kinases of varicella-zoster virus determine tropism for human T cells and skin in the SCID-hu mouse. Proc. Natl. Acad. Sci. USA 95 (1998) 11969-11974.
• 4.Kinchington, P.R., Fite, K., Seman, A. and Turse, S.E. Virion association of IE62, the varicella-zoster virus (VZV) major transcriptional regulatory protein, requires expression of the VZV open reading frame 66 protein kinase. J. Virol. 75 (2001) 9106-9113.
• 5.Kinchington, P.R., Fite, K. and Turse, S.E. Nuclear accumulation of IE62, the varicella-zoster virus (VZV) major transcriptional regulatory protein, is Inhibited by phosphorylation mediated by the VZV open reading frame 66 protein kinase. J. Virol. 74 (2000) 2265-2277.
• 6.Ye, M., Duus, K.M., Peng, J., Price, D.H. and Grose, C. Varicella-zoster virus Fc receptor component gI is phosphorylated on its endodomain by a cyclin-dependent kinase. J. Virol. 73 (1999) 1320-1330.
• 7.Wang, Z.-H., Gershon, M.D., Lungu, O., Zhu, Z., Mallory, S., Arvin, A.M. and Gershon, A.A. Essential role played by the C-terminal domain of glycoprotein I in envelopment of varicella-zoster virus in the trans-Golgi network: Interactions of glycoproteins with tegument. J. Virol. 75 (2001) 323-340.
• 8.Moffat, J.F., Ito, H., Sommer, M., Taylor, S. and Arvin, A.M. Glycoprotein I of varicella-zoster virus is required for viral replication in skin and T cells. J. Virol. 76 (2002) 8468-8471.
• 9.Mallory, S., Sommer, M. and Arvin, A.M. Analysis of the glycoproteins I and E of varicella-zoster virus (VZV) using deletional mutations of VZV cosmids. J. Infect. Dis. 178 Suppl 1 (1998) S22-26.
• 10.Mallory, S., Sommer, M. and Arvin, A.M. Mutational analysis of the role of glycoprotein I in varicella-zoster virus replication and its effects on glycoprotein E conformation and trafficking. J. Virol. 71 (1997) 8279-8288.
• 11.Beshnan, W.A., Albrecht, T. and Thompson, E.A. The cyclin E promoter is activated by human cytomegalovirus 86-kDa immediate early protein. J. Biol. Chem. 273 (1998) 22075-22082.
• 12.Bresnahan, W.A., Boldogh, I., Thompson, E.A. and Albrecht, T. Human cytomegalovirus inhibits cellular DNA synthesis and arrests productively infected cells in late G1. Virology 224 (1996) 150-160.
• 13.Bresnahan, W.A., Thompson, E.A. and Albrecht, T. Human cytomegalovirus infection results in altered Cdk2 subcellular localization. J. Gen. Virol. 78 (1997) 1993-1997.