ArticleJapanese journal of cancer research : Gann1992
Differential expression of subspecies of polyomavirus and murine leukemia virus enhancer core binding protein, PEBP2, in various hematopoietic cells.
Article in Japanese journal of cancer research : Gann, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 46 citations in OpenAlex.
- 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
- The Runx1 transcription factor controls CSF-1-dependent and -independent growth and survival of macrophages.Oncogene · 2005Article
- Oncogenic potential of the RUNX gene family: 'overview'.Oncogene · 2004Review
- Transcriptional regulation of myelopoiesis.International journal of hematology · 2002Review
- Review
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- Sequence-specific and/or stereospecific constraints of the U3 enhancer elements of MCF 247-W are important for pathogenicity.Journal of virology · 1999Article
- The leukemic protein core binding factor beta (CBFbeta)-smooth-muscle myosin heavy chain sequesters CBFalpha2 into cytoskeletal filaments and aggregates.Molecular and cellular biology · 1998Article
- In vivo footprinting of the enhancer sequences in the upstream long terminal repeat of Moloney murine leukemia virus: differential binding of nuclear factors in different cell types.Journal of virology · 1998Article
- An AML-1 consensus sequence binds an osteoblast-specific complex and transcriptionally activates the osteocalcin gene.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Structural alterations in the transcription factor PEBP2/CBF linked to four different types of leukemia.Journal of cancer research and clinical oncology · 1996Review
- Conservation and function of the transcriptional regulatory protein Runt.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Alternative splicing and genomic structure of the AML1 gene involved in acute myeloid leukemia.Nucleic acids research · 1995Article
- Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias.Molecular and cellular biology · 1995Article
- Expression of the Runt domain-encoding PEBP2 alpha genes in T cells during thymic development.Molecular and cellular biology · 1995Article
- An acute myeloid leukemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms.The EMBO journal · 1995Article
- PEBP2/CBF, the murine homolog of the human myeloid AML1 and PEBP2 beta/CBF beta proto-oncoproteins, regulates the murine myeloperoxidase and neutrophil elastase genes in immature myeloid cells.Molecular and cellular biology · 1994Article
- PEBP2/PEA2 represents a family of transcription factors homologous to the products of the Drosophila runt gene and the human AML1 gene.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
- The t(8;21) translocation in acute myeloid leukemia results in production of an AML1-MTG8 fusion transcript.The EMBO journal · 1993Article
- Cloning and characterization of subunits of the T-cell receptor and murine leukemia virus enhancer core-binding factor.Molecular and cellular biology · 1993Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The core sequence of the enhancer of murine leukemia virus (MuLV) long terminal repeat is highly conserved in a large number of MuLV strains and appears to play an essential role when SL3-3 or Moloney strains induce T cell lymphoma in mice. We found by using the electrophoretic mobility shift assay that a polyomavirus enhancer core-binding protein, PEBP2, bound to this core motif of MuLV. We also noted that PEBP2 in several hematopoietic cell lines derived from B lymphocyte, macrophage and myelocyte lineages migrated significantly faster than the authentic PEBP2 detected in NIH3T3 fibroblasts. Interestingly, PEBP2 detected in the cell lines of T lymphocyte lineage appeared to contain both types, which were indistinguishable in electrophoretic mobility from those of NIH3T3 and of B lymphocyte, macrophage and myelocyte lineages. The treatment of the nuclear extract containing PEBP2 with phosphatase generated PEBP3, which is a subcomponent of PEBP2 and retained the same DNA-binding specificity as PEBP2. The altered mobility of hematopoietic cell-derived or T lymphocyte-derived PEBP2 was found to be due to the alteration of the mobility of PEBP3. Based on the distinct mobility of PEBP2/3 of T lymphocytes from those of other hematopoietic cells, we discuss the implication of PEBP2 in MuLV-induced T cell leukemia and T cell-specific gene expression.
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