Regulation of CD40 and CD40 ligand by the AT-hook transcription factor AKNA

Aisha Siddiqa, Jennifer C. Sims-Mourtada, Liliana Guzman-Rojas, Roberto Rangel, Christiane Guret, Vicente Madrid-Marina, Yan Sun and Hector Martinez-Valdez ()
Additional contact information
Aisha Siddiqa: Box 178, The University of Texas M. D. Anderson Cancer Center
Jennifer C. Sims-Mourtada: Box 178, The University of Texas M. D. Anderson Cancer Center
Liliana Guzman-Rojas: Box 178, The University of Texas M. D. Anderson Cancer Center
Roberto Rangel: Box 178, The University of Texas M. D. Anderson Cancer Center
Christiane Guret: Laboratory for Immunology Research, Schering-Plough
Vicente Madrid-Marina: Centro de Investigacion Sobre Enfermedades Infecciosas, Instituto Nacional de Salud Publica
Yan Sun: Box 178, The University of Texas M. D. Anderson Cancer Center
Hector Martinez-Valdez: Box 178, The University of Texas M. D. Anderson Cancer Center

Nature, 2001, vol. 410, issue 6826, 383-387

Abstract: Abstract Proteins containing AT hooks bind A/T-rich DNA through a nine-amino-acid motif and are thought to co-regulate transcription by modifying the architecture of DNA, thereby enhancing the accessibility of promoters to transcription factors1,2. Here we describe AKNA, a human AT-hook protein that directly binds the A/T-rich regulatory elements of the promoters of CD40 and CD40 ligand (CD40L) and coordinately regulates their expression. Consistent with its function, AKNA is a nuclear protein that contains multiple PEST protein-cleavage motifs, which are common in regulatory proteins with high turnover rates3. AKNA is mainly expressed by B and T lymphocytes, natural killer cells and dendritic cells. During B-lymphocyte differentiation, AKNA is mainly expressed by germinal centre B lymphocytes, a stage in which receptor and ligand interactions are crucial for B-lymphocyte maturation4,5,6,7,8,9,10,11,12. Our findings show that an AT-hook molecule can coordinately regulate the expression of a key receptor and its ligand, and point towards a molecular mechanism that explains homotypic cell interactions.

Date: 2001
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DOI: 10.1038/35066602

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