Expression of K13/v-FLIP Gene of Human Herpesvirus 8 and Apoptosis in Kaposi's Sarcoma Spindle Cells

Stürzl, Michael; Hohenadl, Christine; Zietz, Christian; Castaños‐Vélez, Esmeralda; Wunderlich, A; Ascherl, Gudrun; Biberfeld, Peter; Monini, Paolo; Browning, Philip J.; Ensoli, Barbara

doi:10.1093/jnci/91.20.1725

Cited by 157 publications

(111 citation statements)

References 54 publications

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“…44,70 The tumorigenic interplay of these two viruses is mediated by the same ICs that have been shown to induce GBP-1 expression, and expression of all these cytokines has been demonstrated in KS tissue sections. 22,[37][38][39][40][41][42][43][44] In addition, in psoriasis and adverse drug reactions of the skin IFN-␥ expression has been detected.…”

Section: Discussionmentioning

confidence: 99%

Guanylate-Binding Protein-1 Expression Is Selectively Induced by Inflammatory Cytokines and Is an Activation Marker of Endothelial Cells during Inflammatory Diseases

Lubeseder‐Martellato

Guenzi

Jörg

et al. 2002

The American Journal of Pathology

133

140

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During angiogenesis and inflammatory processes, endothelial cells acquire different activation phenotypes, whose identification may help in understanding the complex network of angiogenic and inflammatory interactions in vivo. To this goal we investigated the expression of the human guanylatebinding protein (GBP)-1 that is highly induced by inflammatory cytokines (ICs) and, therefore, may characterize IC-activated cells. Using a new rat monoclonal antibody raised against GBP-1, we show that GBP-1 is a cytoplasmic protein and that its expression in endothelial cells is selectively induced by interferon-␥, interleukin-1␣, interleukin-1␤, or tumor necrosis factor-␣, but not by other cytokines, chemokines, or growth factors. Moreover, we found that GBP-1 expression is highly associated with vascular endothelial cells as confirmed by the simultaneous detection of GBP-1 and the endothelial cell-associated marker CD31 in a broad range of human tissues. Notably, GBP-1 expression was undetectable in the skin, but it was highly induced in vessels of skin diseases with a high-inflammatory component including pso-

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Section: Discussionmentioning

confidence: 99%

Guanylate-Binding Protein-1 Expression Is Selectively Induced by Inflammatory Cytokines and Is an Activation Marker of Endothelial Cells during Inflammatory Diseases

Lubeseder‐Martellato

Guenzi

Jörg

et al. 2002

The American Journal of Pathology

133

140

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“…We subsequently showed that K13 protein also possesses the ability to activate the NF-kB pathway (Chaudhary et al, 1999b;Liu et al, 2002). As K13 is one of the few HHV-8-encoded proteins to be expressed in latently infected KS spindle cells (Sarid et al, 1998;Sturzl et al, 1999), in this report we have investigated its role in the upregulation of IL-8 expression and secretion and the signaling pathways involved in this process.…”

Section: Introductionmentioning

confidence: 95%

Induction of IL-8 expression by human herpesvirus 8 encoded vFLIP K13 via NF-κB activation

Sun

Matta

et al. 2006

Oncogene

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“…As discussed previously, KSHV ORFs 73, 72 and K13 are transcribed as a tricistron from the same promoter, P127880 in KSHV-infected cells. Since this tricistron has one 5′ ss, but two alternative 3′ ss (Figure 2), splicing of an intron of 499 nts from the tricistron leads to the selection of a 5′ ss proximal 3′ ss and results in production of the spliced tricistronic transcript (ORF73/72/K13) predominately responsible for LANA 1 translation [47,58,59]. However, the majority of the tricistrons splice over to the distal 3′ ss by removing a 4 kb intron, and consequently produce the bicistronic transcript (ORF72/K13) responsible for v-cyclin and v-FLIP translation.…”

Section: Mechanisms Possibly Involved In the Regulation Of Kshv Rna Smentioning

confidence: 99%

Split genes and their expression in Kaposi's sarcoma‐associated herpesvirus

Zheng

2003

Reviews in Medical Virology

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SUMMARYA split or interrupted gene is defined as a gene consisting of introns and exons. Removal (splicing) of the intron (s) from a primary transcript (pre-mRNA) is an essential process to create a mRNA. Initial assignment of a potential protein coding region in KSHV genome was based on initiation codon context and predicted protein size larger than 100 amino acids, but the gene discontinuity was disregarded. Experimental investigation of the assigned ORFs has demonstrated that there are up to 25 split genes, more than one fourth of the total KSHV genes described in KSHV genome. This includes the genes involved in all phases (latent, immediate early, early and late) of KSHV infection. The complexity of a split gene expression depends upon the availability of a proximal promoter and polyadenylation (pA) signal. Sharing a single promoter or a single pA signal by two or three genes is not uncommon in the expression of KSHV split genes and the resulting transcripts are usually polycistronic. Among those of KSHV split genes, 15 genes express a bicistronic or tricistronic RNA and 10 genes express a monocistronic RNA. Alternative RNA splicing could happen in a particular pre-mRNA due to intron or exon inclusion or skipping or the presence of an alternative 5′ ss or 3′ ss. This may, respectively, result in at least 8 species of K8 and 14 species of K15 transcripts. This appears to be related to cell differentiation and stages of the virus infection, presumably involving in viral cis elements and trans splicing factors.

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Expression of K13/v-FLIP Gene of Human Herpesvirus 8 and Apoptosis in Kaposi's Sarcoma Spindle Cells

Abstract: These data suggest that functional v-FLIP is produced in vivo and that antiapoptotic mechanisms may be involved in the rapid growth of KS lesions, where only a few cells undergoing mitosis are generally observed.

Cited by 157 publications

References 54 publications

Guanylate-Binding Protein-1 Expression Is Selectively Induced by Inflammatory Cytokines and Is an Activation Marker of Endothelial Cells during Inflammatory Diseases

Guanylate-Binding Protein-1 Expression Is Selectively Induced by Inflammatory Cytokines and Is an Activation Marker of Endothelial Cells during Inflammatory Diseases

Induction of IL-8 expression by human herpesvirus 8 encoded vFLIP K13 via NF-κB activation

Split genes and their expression in Kaposi's sarcoma‐associated herpesvirus

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