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Gene Review

BoHV4gp72  -  v-FLIP

Bovine herpesvirus 4

 
 
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Disease relevance of BoHV4gp72

  • HHV-8-encoded viral Fas-associated death domain-like IL-1-converting enzyme inhibitory protein (vFLIP) is one of the few viral proteins to be expressed in latently infected cells and plays a key role in the survival and proliferation of primary effusion lymphoma cells [1].
  • Activation of NF-kappaB by the latent vFLIP gene of Kaposi's sarcoma-associated herpesvirus is required for the spindle shape of virus-infected endothelial cells and contributes to their proinflammatory phenotype [2].
  • RESULTS: We present evidence that vFLIP K13 activates HIV-1 LTR via the activation of the classical NF-kappaB pathway involving c-Rel, p65 and p50 subunits [3].
 

High impact information on BoHV4gp72

  • HHV8 encodes for a viral FLICE-inhibitory protein (vFLIP), designated K13, which resembles the prodomain of caspase-8 in structure and has been shown to protect cells against death receptor-induced apoptosis in vitro and in vivo [4].
  • To elucidate the mechanism of NF-kappaB activation in PEL cell lines, we have investigated the role of viral FLICE inhibitory protein (vFLIP) in this process [5].
  • Gene silencing experiments by RNA interference demonstrate that vFLIP in BCBL-1 endogenously infected primary effusion lymphoma (PEL) cells mediates JNK/AP1 activation and cIL-6 expression [6].
  • Consistent with this, the inhibition of NF-kappaB activation blocks vFLIP-induced spindling in cultured endothelial cells. vFLIP expression in spindle cells also induces the production of a variety of proinflammatory cytokines and cell surface adhesion proteins that likely contribute to the inflammatory component of KS lesions [2].
  • Here we report that the spindling phenotype involves major rearrangement of the actin cytoskeleton and can be attributed to the expression of a single viral protein, vFLIP, a known activator of NF-kappaB [2].
 

Biological context of BoHV4gp72

  • The three genes encoded by these ORFs (for vFLIP, vCyclin, and latency-associated nuclear antigen [LANA]) are transcribed from a common transcription start site in BCP-1 cells during both latency and the lytic cycles [7].
  • Deregulation of the NF-kappaB pathway is an important strategy used by KSHV to promote lymphoma cell survival, and the viral protein vFLIP is essential for this process [8].
  • By Northern analysis and RT-PCR, we found that MAP30 downregulates the expression of viral cyclin D (vCD), viral interleukin-6 (vIL-6), and viral FLIP (vFLIP), genes involved in cell cycle regulation, viral pathogenesis, and apoptosis [9].
 

Anatomical context of BoHV4gp72

 

Analytical, diagnostic and therapeutic context of BoHV4gp72

  • Immunofluorescence antibody staining revealed that the insertion of a transposon cassette into LNA disrupted its expression but had no effect on the expression of two adjacent genes, the vCyclin and vFLIP genes [11].

References

  1. Constitutive NF-kappaB activation, normal Fas-induced apoptosis, and increased incidence of lymphoma in human herpes virus 8 K13 transgenic mice. Chugh, P., Matta, H., Schamus, S., Zachariah, S., Kumar, A., Richardson, J.A., Smith, A.L., Chaudhary, P.M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  2. Activation of NF-kappaB by the latent vFLIP gene of Kaposi's sarcoma-associated herpesvirus is required for the spindle shape of virus-infected endothelial cells and contributes to their proinflammatory phenotype. Grossmann, C., Podgrabinska, S., Skobe, M., Ganem, D. J. Virol. (2006) [Pubmed]
  3. Kaposi's sarcoma associated herpes virus-encoded viral FLICE inhibitory protein activates transcription from HIV-1 Long Terminal Repeat via the classical NF-kappaB pathway and functionally cooperates with Tat. Sun, Q., Matta, H., Chaudhary, P.M. Retrovirology (2005) [Pubmed]
  4. The human herpes virus 8-encoded viral FLICE-inhibitory protein induces cellular transformation via NF-kappaB activation. Sun, Q., Zachariah, S., Chaudhary, P.M. J. Biol. Chem. (2003) [Pubmed]
  5. The human herpes virus 8-encoded viral FLICE inhibitory protein physically associates with and persistently activates the Ikappa B kinase complex. Liu, L., Eby, M.T., Rathore, N., Sinha, S.K., Kumar, A., Chaudhary, P.M. J. Biol. Chem. (2002) [Pubmed]
  6. Kaposi's sarcoma-associated herpesvirus encoded vFLIP induces cellular IL-6 expression: the role of the NF-kappaB and JNK/AP1 pathways. An, J., Sun, Y., Sun, R., Rettig, M.B. Oncogene (2003) [Pubmed]
  7. Kaposi's sarcoma-associated herpesvirus vCyclin open reading frame contains an internal ribosome entry site. Bieleski, L., Talbot, S.J. J. Virol. (2001) [Pubmed]
  8. Kaposi sarcoma-associated herpesvirus and other viruses in human lymphomagenesis. Cesarman, E., Mesri, E.A. Curr. Top. Microbiol. Immunol. (2007) [Pubmed]
  9. Anti-HIV agent MAP30 modulates the expression profile of viral and cellular genes for proliferation and apoptosis in AIDS-related lymphoma cells infected with Kaposi's sarcoma-associated virus. Sun, Y., Huang, P.L., Li, J.J., Huang, Y.Q., Zhang, L., Huang, P.L., Lee-Huang, S. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
  10. A polypyrimidine tract facilitates the expression of Kaposi's sarcoma-associated herpesvirus vFLIP through an internal ribosome entry site. Bieleski, L., Hindley, C., Talbot, S.J. J. Gen. Virol. (2004) [Pubmed]
  11. Disruption of Kaposi's sarcoma-associated herpesvirus latent nuclear antigen leads to abortive episome persistence. Ye, F.C., Zhou, F.C., Yoo, S.M., Xie, J.P., Browning, P.J., Gao, S.J. J. Virol. (2004) [Pubmed]
 
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