Transcriptional regulation of the human FPR2/ALX gene: evidence of a heritable genetic variant that impairs promoter activity

• Published in: The FASEB journal Vol. 26; no. 3; p. 1323
• Main Authors: Simiele, Felice, Recchiuti, Antonio, Mattoscio, Domenico, De Luca, Antonella, Cianci, Eleonora, Franchi, Sara, Gatta, Valentina, Parolari, Alessandro, Werba, Josè Pablo, Camera, Marina, Favaloro, Bartolo, Romano, Mario
• Format: Journal Article
• Language: English
• Published: United States 01.03.2012
• Subjects: Base Sequence; Binding Sites - genetics; Blotting, Western; Cell Line; Cell Line, Tumor; DNA Methylation; Gene Expression Regulation; Genetic Variation; Humans; Models, Genetic; Molecular Sequence Data; Polymorphism, Single Nucleotide; Promoter Regions, Genetic - genetics; Protein Binding; Receptors, Formyl Peptide - genetics; Receptors, Formyl Peptide - metabolism; Receptors, Lipoxin - genetics; Receptors, Lipoxin - metabolism; Reverse Transcriptase Polymerase Chain Reaction; Sp1 Transcription Factor - metabolism; Transcription Initiation Site; Transcription, Genetic - genetics

Lipoxin (LX) A(4,) a main endogenous stop-signal of inflammation, activates the G-protein-coupled receptor FPR2/ALX, which triggers potent anti-inflammatory signaling in vivo. Thus, the regulation of FPR2/ALX expression may have pathophysiological and therapeutic relevance. Here, we mapped a nucleot...