Exogenous Nucleosides Promote the Completion of MoMLV DNA Synthesis in G0-Arrested Balb c/3T3 Fibroblasts

Goulaouic, Hélène; Subra, Frédéric; Mouscadet, Jean François; Carteau, Sandrine; Auclair, Christian

doi:10.1006/viro.1994.1166

Cited by 32 publications

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“…It has been shown that HBV replication depends on cell cycle and di erentiation status and is decreased in S phase (Ozer et al, 1996). Thus, maintenance of activated cells in late G1 might favor further rounds of HBV-DNA replication by inducing expression of liver speci®c transcription and replication factors, as increasing the pool of free dNTPs (Goulaoui et al, 1994). In this view, the late induction of apoptosis might re¯ect prolonged expression of HBx in cells blocked at G1/S phase.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus X mutants, present in hepatocellular carcinoma tissue abrogate both the antiproliferative and transactivation effects of HBx

et al. 1999

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Chronic infection by HBV is the leading cause of hepatocellular carcinoma in man. Several lines of evidence suggest that the viral transactivator HBx plays a critical role in the molecular pathogenesis of HBVrelated HCC. To study the actual impact of HBx and the mechanism of its action, we have recently cloned and characterized a set of X-sequences from HCC in patients with chronic infection by HBV. In the present study, we have compared the e ects of HBx and its naturally arising mutants on cell growth and viability. We report that HBx inhibits clonal outgrowth of cells and induces apoptosis by a p53-independent pathway. Furthermore, HBx expression induced a late G1 cell cycle block prior to their counterselection by apoptosis. Importantly, mutations in the HBx-gene evolving in hepatocellular carcinoma abolished both HBx-induced growth arrest and apoptosis. Using a panel of engineered mutants we have mapped the growth suppressive e ect of HBx to domains shown to be required for its transactivating function. Based on these results, we propose that abrogation of the anti-proliferative and apoptotic e ects of HBx by naturally occurring mutations might render the hepatocytes susceptible to uncontrolled growth and contribute to multistep hepatocarcinogenesis associated with HBV-infection.

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Section: Discussionmentioning

confidence: 99%

Hepatitis B virus X mutants, present in hepatocellular carcinoma tissue abrogate both the antiproliferative and transactivation effects of HBx

et al. 1999

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“…In contrast, if HBx were to function as a TAF II 250-like protein, promoting cells into cycling, this would be deleterious, as studies have shown greatly impaired HBV replication in cells during S phase (57). Importantly, for classic retroviruses, depletion of dNTP pools, particularly dCTP, has been shown to be responsible for arrest of viral reverse transcription in G 0 cells, which is relieved by transit into the G 1 -S transition or by supplementation of G 0 -arrested cells with high levels of dNTPs (13,25,26,93,94). HBx has been shown to be required for HBV replication (12,95), which also utilizes reverse transcription of the viral RNA genome.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B Virus HBx Protein Activation of Cyclin A–Cyclin-Dependent Kinase 2 Complexes and G ₁ Transit via a Src Kinase Pathway

Bouchard

Giannakopoulos

Wang

et al. 2001

J Virol

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“…Ksp1 and shm1 mutants had wild type or greater amounts plex of pol III (Kirchner et al 1995;Yieh et al 2000), binding of these factors or access to the target could of cDNA but were both Ͻ50% of wild-type transposition into the tDNAVal (AAC) target. Ksp1p is a S/T kinase and be affected by local chromatin structure.…”

Section: Analysis Of Ty3 Cdna In Mutant Strains: Subsequentmentioning

confidence: 99%

“…In the case of retroviruses, exogenous nucleoout collection. Scholes et al (2001) found that most of the identified disruptions yielded elevated transposition sides can promote the completion of DNA synthesis in G 0 -arrested fibroblasts (Goulaouic et al 1994; Kootsand were in DNA checkpoint, repair, and telomere maintenance genes. The screen by Griffith et al (2003Griffith et al ( ) recovtra et al 2000.…”

Section: Analysis Of Ty3 Cdna In Mutant Strains: Subsequentmentioning

confidence: 99%

Host Factors That Affect Ty3 Retrotransposition in Saccharomyces cerevisiae

et al. 2004

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The retrovirus-like element Ty3 of Saccharomyces cerevisiae integrates at the transcription initiation region of RNA polymerase III. To identify host genes that affect transposition, a collection of insertion mutants was screened using a genetic assay in which insertion of Ty3 activates expression of a tRNA suppressor. Fifty-three loci were identified in this screen. Corresponding knockout mutants were tested for the ability to mobilize a galactose-inducible Ty3, marked with the HIS3 gene. Of 42 mutants tested, 22 had phenotypes similar to those displayed in the original assay. The proteins encoded by the defective genes are involved in chromatin dynamics, transcription, RNA processing, protein modification, cell cycle regulation, nuclear import, and unknown functions. These mutants were induced for Ty3 expression and assayed for Gag3p protein, integrase, cDNA, and Ty3 integration upstream of chromosomal tDNA Val(AAC) genes. Most mutants displayed differences from the wild type in one or more intermediates, although these were typically not as severe as the genetic defect. Because a relatively large number of genes affecting retrotransposition can be identified in yeast and because the majority of these genes have mammalian homologs, this approach provides an avenue for the identification of potential antiviral targets.

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Exogenous Nucleosides Promote the Completion of MoMLV DNA Synthesis in G0-Arrested Balb c/3T3 Fibroblasts

Cited by 32 publications

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Hepatitis B virus X mutants, present in hepatocellular carcinoma tissue abrogate both the antiproliferative and transactivation effects of HBx

Hepatitis B virus X mutants, present in hepatocellular carcinoma tissue abrogate both the antiproliferative and transactivation effects of HBx

Hepatitis B Virus HBx Protein Activation of Cyclin A–Cyclin-Dependent Kinase 2 Complexes and G ₁ Transit via a Src Kinase Pathway

Host Factors That Affect Ty3 Retrotransposition in Saccharomyces cerevisiae

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Exogenous Nucleosides Promote the Completion of MoMLV DNA Synthesis in G0-Arrested Balb c/3T3 Fibroblasts

Cited by 32 publications

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Hepatitis B virus X mutants, present in hepatocellular carcinoma tissue abrogate both the antiproliferative and transactivation effects of HBx

Hepatitis B virus X mutants, present in hepatocellular carcinoma tissue abrogate both the antiproliferative and transactivation effects of HBx

Hepatitis B Virus HBx Protein Activation of Cyclin A–Cyclin-Dependent Kinase 2 Complexes and G 1 Transit via a Src Kinase Pathway

Host Factors That Affect Ty3 Retrotransposition in Saccharomyces cerevisiae

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Hepatitis B Virus HBx Protein Activation of Cyclin A–Cyclin-Dependent Kinase 2 Complexes and G ₁ Transit via a Src Kinase Pathway