Reports outline biochemistry study findings from University Complutense of Madrid
2007 AUG 13 -- New research, "Effect of diadenosine polyphosphates in achondroplasic chondrocytes: inhibitory effect of Ap4A on FGF9 induced MAPK cascade," is the subject of a report. "Achondroplasia is characterised by a mutation in the gene that encodes for the FGF receptor type 3 (FGFR3), producing a hyperactivation of this receptor and a subsequent increase in MAPK activity. We have tested the ability of nucleotides to decrease the activation of MAPK in chondrocytes with achondroplasic FGFR3 receptor," investigators in Madrid, Spain report. "Diadenosine tetraphosphate, Ap(4)A, reduced the phosphorylation of pERK1/2 triggered by FGF9 (38% reduction). Ap(4)A diminished the expression of achondroplasic FGFR3 receptor (65% reduction), stimulating FGFR3 receptor degradation," wrote A. Guzmán-Aránguez and colleagues, University Complutense of Madrid. The researchers concluded: "The action of Ap(4)A seems to be mediated by a dinucleotide receptor rather than by any other ATP receptor." Guzmán-Aránguez and colleagues published their study in Biochemical Pharmacology (Effect of diadenosine polyphosphates in achondroplasic chondrocytes: inhibitory effect of Ap4A on FGF9 induced MAPK cascade. Biochemical Pharmacology, 2007;74(3):448-56). For additional information, contact A. Guzmán-Aránguez, Universidad Complutense de Madrid, Departamento de Bioquimica y Biologia Molecular IV, EU Optica, c, Arcos de Jalon s, n, 28037 Madrid, Spain. The publisher of the journal Biochemical Pharmacology can be contacted at: Pergamon-Elsevier Science Ltd., the Boulevard, Langford Lane, Kidlington, Oxford OX5 1GB, England. Keywords: Spain, Madrid, Biochemistry, Biochemical Pharmacology, Pharmaceuticals. This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2007, Biotech Business Week via NewsRx.com.
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