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M004323200v1
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Papers In Press, published online ahead of print July 5, 2000
J. Biol. Chem, 10.1074/jbc.M004323200
Submitted on May 19, 2000
Accepted on July 4, 2000

Polyomavirus Enhancer Binding protein 2 (PEBP2)/Core Binding Factor (CBF)/AML factors contribute to the cell type-specific activity of the CD11a integrin gene promoter

Amaya Puig-Kroger, Cristina Lopez-Rodriguez, Miguel Relloso, Tilman Sanchez-Elsner, Arsenio Nueda, Eduardo Munoz, Carmelo Bernabeu, and Angel L. Corbi

Dept. of Immunology, Consejo Superior de Investigaciones Cientificas, Madrid, Madrid 28006

Corresponding Author: acorbi{at}cib.csic.es

The CD11a/CD18 leukocyte integrin (LFA-1; alpha L/beta 2) 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 on 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 while the effect was considerably lower in K562 and HepG2 cells. Electrophoretic mobility shift assays (EMSA) evidenced cell type-specific differences in CD11a-110 binding and indicated its specific recognition by members of the Polyomavirus Enhancer Binding Protein 2 (PEBP2)/Core Binding Factor (CBF)/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.


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