Findings from INSERM advance knowledge in dysplasia
2007 JUL 17 -- Scientists discuss in "Human immortalized chondrocytes carrying heterozygous FGFR3 mutations: an in vitro model to study chondrodysplasias" new findings in dysplasia. According to a study from Paris, France, "Achondroplasia and thanatophoric dysplasia are human chondrodysplasias caused by mutations in the fibroblast growth factor receptor 3 (FGFR3) gene. We have developed an immortalized human chondrocyte culture model to study the regulation of chondrocyte functions." "One control and eight mutant chondrocytic lines expressing different FGFR3 heterozygous mutations were obtained. FGFR3 signaling pathways were modified in the mutant lines as revealed by the constitutive activation of the STAT pathway and an increased level of P21(WAF1/CIP1) protein," wrote C. Benoist-Lasselin and colleagues, INSERM. The researchers concluded: "This model will be useful for the study of FGFR3 function in cartilage studies and future therapeutic approaches in chondrodysplasias." Benoist-Lasselin and colleagues published their study in FEBS Letters (Human immortalized chondrocytes carrying heterozygous FGFR3 mutations: an in vitro model to study chondrodysplasias. FEBS Letters, 2007;581(14):2593-8). For more information, contact C. Benoist-Lasselin, INSERM U781, Hopital Necker-Enfants Malades, 149 rue de Sevres, Paris, France. Publisher contact information for the journal FEBS Letters is: Elsevier Science BV, PO Box 211, 1000 AE Amsterdam, Netherlands. Keywords: France, Paris, Dermatology, Dysplasia. This article was prepared by Life Science Weekly editors from staff and other reports. Copyright 2007, Life Science Weekly via NewsRx.com.
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