{"title":"通过共表达分析鉴定细胞粘附和基质重塑基因","authors":"Michael G. Walker, Wayne Volkmuth","doi":"10.1002/gnfd.200290000","DOIUrl":null,"url":null,"abstract":"<p>Cell adhesion and matrix remodeling are elements in many diseases, ranging from atherosclerosis and fibrosis to metastatic cancer. However, many genes that participate in these processes have not yet been identified. To find such genes, we looked for previously uncharacterized genes that are co-expressed with known cell adhesion and matrix remodeling genes. The known genes in this study included MMP2, TIMP3, BM-40, chondroitin, connective tissue growth factor, fibromodulin, IGFBP5, laminin, MGP, myosin light chain kinase, several collagens, and other matrix and adhesion proteins. We found eight previously uncharacterized genes, here named MXRA1 through MXRA8, that were strongly co-expressed with these known adhesion and matrix genes. Five of the MXRA genes have a significant similarity to uncharacterized cDNA sequences or predicted proteins listed in the Genbank database, but otherwise show distant or no sequence similarity to genes with known function. Subsequent to our entry of the MXRA gene sequences in the Genbank, three of the eight genes have been independently described by other researchers: MXRA2 is α-parvin, a cell-matrix adhesion protein, MXRA4 is a C1 complement component receptor involved in cell adhesion, and MXRA5 is adlican, an adhesion proteoglycan. The analysis described here provides further evidence for the role of these genes in adhesion and matrix remodeling.</p>","PeriodicalId":100573,"journal":{"name":"Gene Function & Disease","volume":"3 3-4","pages":"109-112"},"PeriodicalIF":0.0000,"publicationDate":"2003-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/gnfd.200290000","citationCount":"27","resultStr":"{\"title\":\"Cell adhesion and matrix remodeling genes identified by co-expression analysis\",\"authors\":\"Michael G. Walker, Wayne Volkmuth\",\"doi\":\"10.1002/gnfd.200290000\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Cell adhesion and matrix remodeling are elements in many diseases, ranging from atherosclerosis and fibrosis to metastatic cancer. However, many genes that participate in these processes have not yet been identified. To find such genes, we looked for previously uncharacterized genes that are co-expressed with known cell adhesion and matrix remodeling genes. The known genes in this study included MMP2, TIMP3, BM-40, chondroitin, connective tissue growth factor, fibromodulin, IGFBP5, laminin, MGP, myosin light chain kinase, several collagens, and other matrix and adhesion proteins. We found eight previously uncharacterized genes, here named MXRA1 through MXRA8, that were strongly co-expressed with these known adhesion and matrix genes. Five of the MXRA genes have a significant similarity to uncharacterized cDNA sequences or predicted proteins listed in the Genbank database, but otherwise show distant or no sequence similarity to genes with known function. Subsequent to our entry of the MXRA gene sequences in the Genbank, three of the eight genes have been independently described by other researchers: MXRA2 is α-parvin, a cell-matrix adhesion protein, MXRA4 is a C1 complement component receptor involved in cell adhesion, and MXRA5 is adlican, an adhesion proteoglycan. The analysis described here provides further evidence for the role of these genes in adhesion and matrix remodeling.</p>\",\"PeriodicalId\":100573,\"journal\":{\"name\":\"Gene Function & Disease\",\"volume\":\"3 3-4\",\"pages\":\"109-112\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2003-01-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1002/gnfd.200290000\",\"citationCount\":\"27\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Gene Function & Disease\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/gnfd.200290000\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gene Function & Disease","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/gnfd.200290000","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Cell adhesion and matrix remodeling genes identified by co-expression analysis
Cell adhesion and matrix remodeling are elements in many diseases, ranging from atherosclerosis and fibrosis to metastatic cancer. However, many genes that participate in these processes have not yet been identified. To find such genes, we looked for previously uncharacterized genes that are co-expressed with known cell adhesion and matrix remodeling genes. The known genes in this study included MMP2, TIMP3, BM-40, chondroitin, connective tissue growth factor, fibromodulin, IGFBP5, laminin, MGP, myosin light chain kinase, several collagens, and other matrix and adhesion proteins. We found eight previously uncharacterized genes, here named MXRA1 through MXRA8, that were strongly co-expressed with these known adhesion and matrix genes. Five of the MXRA genes have a significant similarity to uncharacterized cDNA sequences or predicted proteins listed in the Genbank database, but otherwise show distant or no sequence similarity to genes with known function. Subsequent to our entry of the MXRA gene sequences in the Genbank, three of the eight genes have been independently described by other researchers: MXRA2 is α-parvin, a cell-matrix adhesion protein, MXRA4 is a C1 complement component receptor involved in cell adhesion, and MXRA5 is adlican, an adhesion proteoglycan. The analysis described here provides further evidence for the role of these genes in adhesion and matrix remodeling.