| First Author | Xu P | Year | 2007 |
| Journal | Regul Pept | Volume | 138 |
| Issue | 2-3 | Pages | 51-5 |
| PubMed ID | 17196677 | Mgi Jnum | J:124442 |
| Mgi Id | MGI:3721717 | Doi | 10.1016/j.regpep.2006.11.017 |
| Citation | Xu P, et al. (2007) Alterations in gene expression in the testis of angiotensin-(1-7)-receptor Mas-deficient mice. Regul Pept 138(2-3):51-5 |
| abstractText | The Mas protooncogene encodes a G-protein coupled receptor with seven trans-membrane domains and was recently described as a receptor for angiotensin-(1-7). Mas is highly expressed in testis and brain of rodents, whereas its expression in testis is localized to Leydig cells, being upregulated during puberty. Although the expression of this receptor in testis is strongly ontogenetically controlled and cell type-specific, Mas-deficient mice are fertile. To identify genes of which the expression is affected by the deletion of Mas, we performed differential gene expression profiling. Testis-RNA of Mas-knockout mice on a C57Bl/6 background vs. testis-RNA of C57Bl/6 wild type mice were analyzed on an Affymetrix Murine Genome U74v2 GeneChip probing >12,000 transcripts. The microarray identified 67 transcripts, which were downregulated in Mas-deficient mice and 65 genes, which were upregulated. The analysis of 132 differentially expressed genes by a Gene Ontology Mining Tool revealed genes with activities in mitochondria being overrepresented in the set of significantly affected genes. For some selected genes, the results were verified by a specific real time PCR. Three of these genes, coding for proteins involved in mitochondrial function and steroidogenesis, become henceforth targets for our continuing search for the physiological function of Mas in testis. |
