ArticleJournal of virology1995
Transcriptional activity of core binding factor-alpha (AML1) and beta subunits on murine leukemia virus enhancer cores.
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 34 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
34 citing papers in PubMed, 54 citations in OpenAlex.
- A novel enhancer RNA, Hmrhl, positively regulates its host gene,Non-coding RNA research · 2019Article
- Cbfβ2 controls differentiation of and confers homing capacity to prethymic progenitors.The Journal of experimental medicine · 2018Article
- Core Binding Factor Acute Myeloid Leukemia: New Prognostic Categories and Therapeutic Opportunities.Seminars in hematology · 2015Review
- Aberrant epigenetic regulators control expansion of human CD34+ hematopoietic stem/progenitor cells.Frontiers in genetics · 2013Review
- Article
- Article
- RUNX1 permits E4orf6-directed nuclear localization of the adenovirus E1B-55K protein and associates with centers of viral DNA and RNA synthesis.Journal of virology · 2008Article
- ALY is a common coactivator of RUNX1 and c-Myb on the type B leukemogenic virus enhancer.Journal of virology · 2007Article
- Article
- Review
- 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
- Review
- Type B leukemogenic virus has a T-cell-specific enhancer that binds AML-1.Journal of virology · 2001Article
- Runx2: a novel oncogenic effector revealed by in vivo complementation and retroviral tagging.Oncogene · 2001Article
- Long terminal repeat regions from exogenous but not endogenous feline leukemia viruses transactivate cellular gene expression.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
- 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
- Suppressor mutations within the core binding factor (CBF/AML1) binding site of a T-cell lymphomagenic retrovirus.Journal of virology · 1999Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Core binding factor (CBF), also known as polyomavirus enhancer-binding protein 2 and SL3 enhancer factor 1, is a mammalian transcription factor that binds to an element termed the core within the enhancers of the murine leukemia virus family of retroviruses. The core elements of the SL3 virus are important genetic determinants of the ability of this virus to induce T-cell lymphomas and the transcriptional activity of the viral long terminal repeat in T lymphocytes. CBF consists of two subunits, a DNA binding subunit, CBF alpha, and a second subunit, CBF beta, that stimulates the DNA binding activity of CBF alpha. One of the genes that encodes a CBF alpha subunit is AML1, also called Cbf alpha 2. This locus is rearranged by chromosomal translocations in human myeloproliferative disorders and leukemias. An exogenously expressed Cbf alpha 2-encoded subunit (CBF alpha 2-451) stimulated transcription from the SL3 enhancer in P19 and HeLa cells. Activity was mediated through the core elements. Three different isoforms of CBF beta were also tested for transcriptional activity on the SL3 enhancer. The longest form, CBF beta-187, increased the transcriptional stimulation by CBF alpha 2-451 twofold in HeLa cells, although it had no effect in P19 cells. Transcriptional activation by CBF beta required binding to the CBF alpha subunit, as a form of CBF beta that lacked binding ability, CBF beta-148, failed to increase activity. These results indicated that at least in certain cell types, the maximum activity of CBF required both subunits. They also provided support for the hypothesis that CBF is a factor in T lymphocytes that is responsible for recognition of the SL3 cores. We also examined whether CBF could distinguish a 1-bp difference between the enhancer core of SL3 and the core of the nonleukemogenic virus, Akv. This difference strongly affects transcription in T cells and leukemogenicity of SL3. However, no combination of CBF alpha and CBF beta subunits that we tested was able to distinguish the 1-bp difference in transcription assays. Thus, a complete understanding of how T cells recognize the SL3 core remains to be elucidated.
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