2007
DOI: 10.1111/j.1349-7006.2007.00555.x
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γ‐Herpesviruses and cellular signaling in AIDS‐associated malignancies

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Cited by 11 publications
(11 citation statements)
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References 102 publications
(130 reference statements)
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“…Once adopted, the nonproductive latency program is characterized by constitutive expression of a small subset of KSHV genes, many of which are localized to a single locus [ 2 , 4 , 10 ]. The program is well documented to occur in both virus-harboring KS spindle cells and PEL cells [ 2 , 3 , 4 , 10 , 11 , 12 , 13 , 14 ].…”
Section: Kaposi’s Sarcoma-associated Herpesvirus Latency and Reactmentioning
confidence: 99%
“…Once adopted, the nonproductive latency program is characterized by constitutive expression of a small subset of KSHV genes, many of which are localized to a single locus [ 2 , 4 , 10 ]. The program is well documented to occur in both virus-harboring KS spindle cells and PEL cells [ 2 , 3 , 4 , 10 , 11 , 12 , 13 , 14 ].…”
Section: Kaposi’s Sarcoma-associated Herpesvirus Latency and Reactmentioning
confidence: 99%
“…11 In addition, intracellular Notch1 is elevated in latent phase of HHV-8 in primary effusion lymphoma cell lines, 5 and the increased intracellular Notch1 is potentially able to reactivate HHV-8 from its latency by binding to DNA-binding protein recombination signal sequence-binding protein-J kappa to convert this complex to a positive transcriptional complex from a corepressor complex. 12 In fact, the crystal structure of C promoter binding factor clearly shows that intracellular Notch1 binds the hydrophobic pocket on C promoter binding factor. 13 The expression of Notch1 in primary effusion lymphoma patients may also shed light on the potential therapeutic use of Notch1 inhibitors on primary effusion lymphoma patients.…”
Section: Discussionmentioning
confidence: 99%
“…Further, Furler and Uittenbogaart (2010) argue that cytokine and biomarker expression in HIV-1 infection results from the combined effect of intracellular signaling pathways orchestrated by kinases like p38 and ERK, and that p38, ERK and Mitogen-Activated Protein Kinase (MAPK) pathways govern the regulation of cytokines (IL-2, IL-10, and TNF-α) as well as biomarkers (PD-1, Fas/FasL, among others) that are skewed in chronic HIV infection. Additionally, HIV utilizes the p38 and ERK pathways to produce new virions to deplete Noguchi et al (2007) showed that EBER can activate NF-kB and IRF3 pathways. EBER-mediated signaling has been associated with cytokine expressions in EBV-infected cells.…”
Section: Discussionmentioning
confidence: 99%