Zusammenfassung
The murine gene for CORS-26 shows striking homologies to the adipocyte-specific secretory protein adiponectin (belonging to the newly discovered C1q/TNF molecular superfamily) and its expression has been reported to be restricted to fibroblasts, cartilage and kidney. However, the present data demonstrate specific induction of CORS-26 mRNA expression in hormonally differentiated 3T3-L1 adipocytes, ...
Zusammenfassung
The murine gene for CORS-26 shows striking homologies to the adipocyte-specific secretory protein adiponectin (belonging to the newly discovered C1q/TNF molecular superfamily) and its expression has been reported to be restricted to fibroblasts, cartilage and kidney. However, the present data demonstrate specific induction of CORS-26 mRNA expression in hormonally differentiated 3T3-L1 adipocytes, but not in preadipocytes. Furthermore, CORS-26 mRNA expression could be demonstrated in human synovial adipocytes of the knee by in situ hybridization. Since the genes for CORS-26 and adiponectin are homologous for their COOH-terminal globular domain and of their N-terminal collagenous domain, they might have originated by divergence from an innate mesenchymal precursor molecule directing the development of myocytes, adipocytes and chondrocytes from a mesenchymal stem cell. Here, the complete genomic organization with exon/intron boundaries together with exon-specific primer combinations are presented. Additionally, similar to 1 kb of the TATA-box-containing promoter region was cloned and analyzed for putative transcription factor binding sites. The chromosomal localization of the murine CORS-26 gene was mapped to mouse chromosome 15 A2 by fluorescence in situ hybridization (FISH). Since the linkage loci for proteoglycan-induced arthritis and MRL/lpr arthritis in mice have been mapped to that chromosomal region, CORS-26 might represent the underlying mechanism of disease. The present data provide the basis for further investigation of the CORS-26 gene regulation in the context of mesenchymal tissue development, chondrocyte/adipocyte function and bone or skeletal disease. (C) 2003 Elsevier B.V. All rights reserved.
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