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Polyomavirus enhancer-binding protein 2/core binding factor/acute myeloid leukemia factors contribute to the cell type-specific activity of the CD11a integrin gene promoter

AuthorsPuig-Kröger, Amaya CSIC; López-Rodríguez, Cristina; Relloso, Miguel; Sánchez-Elsner, Tilman; Nueda, Arsenio; Muñoz, Eduardo; Bernabéu, Carmelo CSIC ORCID ; Corbí, Angel L. CSIC ORCID
KeywordsFunction-associated antigen-1
Nuclear factor-i
Transcription factor
Murine myeloperoxidase
Adhesion molecules
Issue Date15-Sep-2000
PublisherAmerican Society for Biochemistry and Molecular Biology
CitationJ Biol Chem 275(37):28507-12 (2000)
AbstractThe CD11a/CD18 leukocyte integrin (LFA-1; also known as alphaL/beta2) mediates leukocyte transendothelial migration during immune and inflammatory responses and participates in lymphoma metastasis. CD11a/CD18 leukocyte-restricted expression is controlled by the CD11a gene promoter, which confers tissue-specific expression to reporter genes in vitro and in vivo. DNase I protection analysis of the CD11a proximal gene promoter revealed DNA-protein interactions centered at position -110 (CD11a-110). Disruption of CD11a-110 reduced CD11a promoter activity in a cell type-specific manner, as it reduced its activity by 70% in Jurkat lymphoid cells, whereas the effect was considerably lower in K562 and HepG2 cells. Electrophoretic mobility shift assays showed evidence of cell type-specific differences in CD11a-110 binding and indicated its specific recognition by members of the polyomavirus enhancer-binding protein 2/core binding factor (CBF)/acute myeloid leukemia (AML) family of transcription factors. AML1B/CBFbeta transactivated the CD11a promoter, with AML1B/CBFbeta-mediated transactivation being completely dependent on the integrity of the CD11a-110 element. Therefore, CBF/AML factors play a role in the cell type-restricted transcription of the CD11a integrin gene through recognition of CD11a-110. The involvement of CBF/AML factors in CD11a expression raises the possibility that CD11a/CD18 expression might be deregulated in acute myeloid and B-lineage acute lymphoblastic leukemias, thus contributing to their altered adhesion and metastatic potential.
Description7 p.-7 fig.1 tab.
Publisher version (URL)http://dx.doi.org/10.1074/jbc.M004323200
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