ArticleJournal of virology1995
Long terminal repeat enhancer core sequences in proviruses adjacent to c-myc in T-cell lymphomas induced by a murine retrovirus.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
40 citing papers in PubMed, 53 citations in OpenAlex.
- Xenotropic Mouse Gammaretroviruses Isolated from Pre-Leukemic Tissues Include a Recombinant.Viruses · 2018Article
- Recombinant Origins of Pathogenic and Nonpathogenic Mouse Gammaretroviruses with Polytropic Host Range.Journal of virology · 2017Article
- Novel principles of gamma-retroviral insertional transcription activation in murine leukemia virus-induced end-stage tumors.Retrovirology · 2014Article
- Control of pathogenicity and disease specificity of a T-lymphomagenic gammaretrovirus by E-box motifs but not by an overlapping glucocorticoid response element.Journal of virology · 2009Article
- Evaluation of binding selectivity of a polyamide probe to single base-pair different DNA in A.T-rich region by electrospray ionization mass spectrometry.Journal of the American Society for Mass Spectrometry · 2006Article
- Leukemia virus long terminal repeat activates NFkappaB pathway by a TLR3-dependent mechanism.Virology · 2006Article
- Substitution of feline leukemia virus long terminal repeat sequences into murine leukemia virus alters the pattern of insertional activation and identifies new common insertion sites.Journal of virology · 2005Article
- Analysis of wild-type and mutant SL3-3 murine leukemia virus insertions in the c-myc promoter during lymphomagenesis reveals target site hot spots, virus-dependent patterns, and frequent error-prone gap repair.Journal of virology · 2005Article
- Article
- Duplication of U3 sequences in the long terminal repeat of mink cell focus-inducing viruses generates redundancies of transcription factor binding sites important for the induction of thymomas.Journal of virology · 2003Article
- What retroviruses teach us about the involvement of c-Myc in leukemias and lymphomas.Leukemia · 2002Review
- Selection for c-myc integration sites in polyclonal T-cell lymphomas.Journal of virology · 2002Article
- Disruption of hematopoiesis and thymopoiesis in the early premalignant stages of infection with SL3-3 murine leukemia virus.Journal of virology · 2002Article
- Ikaros, a lymphoid-cell-specific transcription factor, contributes to the leukemogenic phenotype of a mink cell focus-inducing murine leukemia virus.Journal of virology · 2002Article
- Sint1, a common integration site in SL3-3-induced T-cell lymphomas, harbors a putative proto-oncogene with homology to the septin gene family.Journal of virology · 2000Article
- Increased induction of osteopetrosis, but unaltered lymphomagenicity, by murine leukemia virus SL3-3 after mutation of a nuclear factor 1 site in the enhancer.Journal of virology · 1999Article
- Tandemization of a subregion of the enhancer sequences from SRS 19-6 murine leukemia virus associated with T-lymphoid but not other leukemias.Journal of virology · 1999Article
- Selection of reversions and suppressors of a mutation in the CBF binding site of a lymphomagenic retrovirus.Journal of virology · 1999Article
- Core-binding factor influences the disease specificity of Moloney murine leukemia virus.Journal of virology · 1999Article
- Feline leukemia virus long terminal repeat activates collagenase IV gene expression through AP-1.Journal of virology · 1999Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The transcriptional enhancer in the long terminal repeat (LTR) of the T-lymphomagenic retrovirus SL3-3 differs from that of the nonleukemogenic virus Akv at several sites, including a single base pair difference in an element termed the enhancer core. Mutation of this T-A base pair to the C-G C-G sequence found in Akv significantly attenuated the leukemogenicity of SL3-3. Thus, this difference is important for viral leukemogenicity. Since Akv is an endogenous virus, this suggests that the C-G in its core is an adaptation to being minimally pathogenic. Most tumors that occurred in mice inoculated with the mutant virus, called SAA, contained proviruses with reversion or potential suppressor mutations in the enhancer core. We also found that the 72-bp tandem repeats constituting the viral enhancer could vary in number. Most tumors contained mixtures of proviruses with various numbers of 72-bp units, usually between one and four. Variation in repeat number was most likely due to recombination events involving template misalignment during viral replication. Thus, two processes during viral replication, misincorporation and recombination, combined to alter LTR enhancer structure and generate more pathogenic variants from the mutant virus. In SAA-induced tumors, enhancers of proviruses adjacent to c-myc had the largest number of core reversion or suppressor mutations of all of the viral enhancers in those tumors. This observation was consistent with the hypothesis that one function of the LTR enhancers in leukemogenesis is to activate proto-oncogenes such as c-myc.
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