The novel gene EGFL9/Dlk2, highly homologous to Dlk1, functions as a modulator of adipogenesis |
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Authors: | Nueda María-Luisa Baladrón Victoriano García-Ramírez José-Javier Sánchez-Solana Beatriz Ruvira María-Desamparados Rivero Samuel Ballesteros María-Angeles Monsalve Eva-María Díaz-Guerra María-José M Ruiz-Hidalgo María-José Laborda Jorge |
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Institution: | Department of Inorganic and Organic Chemistry and Biochemistry, Medical School, Regional Center for Biomedical Research, University of Castilla-La Mancha, Albacete, Spain. |
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Abstract: | The Dlk1 gene appears to function as a regulator of adipogenesis. Adult Dlk1-deficient mice are obese, but adipose tissue still develops in transgenic mice overexpressing an Fc-dlk1 fusion protein, and neither type of genetically modified mice displays serious abnormalities. It was therefore possible that one yet unidentified gene might either compensate or antagonize for the absence or for overexpression, respectively, of Dlk1 in those animals. In database searches, we found a novel gene, EGFL9, encoding for a protein whose structural features are virtually identical to those of dlk1, suggesting it may function in a similar way. As dlk1 does, the protein encoded by EGFL9/Dlk2 affects adipogenesis of 3T3-L1 preadipocytes and mesenchymal C3H10T1/2 cells; however, it does so in an opposite way to that of dlk1. In addition, expression levels of both genes appear to be inversely correlated in both cell lines. Moreover, enforced changes in the expression of one gene affect the expression levels of the other. Our data suggest that adipogenesis may be modulated by the coordinated expression of Dlk1 and EGFL9/Dlk2. |
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Keywords: | Dlk1 EGFL9 Dlk2 EGF-like proteins adipogenesis |
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