Genetic and Functional Evidence Supporting SUMO4 as a Type 1 Diabetes Susceptibility Gene
: Genomewide linkage analyses since the early 1990s suggested over 20 genomic intervals that may contain susceptibility genes for type 1 diabetes. However, the identification of the specific genes in these intervals presents a formidable challenge due to a number of difficulties associated with gen...
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| Veröffentlicht in: | Annals of the New York Academy of Sciences 2006-10, Vol.1079 (1), p.257-267 |
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| creator | WANG, CONG-YI PODOLSKY, ROBERT SHE, JIN-XIONG |
| description | : Genomewide linkage analyses since the early 1990s suggested over 20 genomic intervals that may contain susceptibility genes for type 1 diabetes. However, the identification of the specific genes in these intervals presents a formidable challenge due to a number of difficulties associated with genetic mapping and cloning of genes implicated in complex diseases. One of the difficulties is due to the presence of many weak and different susceptibility genes in different patients and populations, a phenomenon known as genetic heterogeneity. In 2004, we reported the cloning of a novel small ubiquitin‐like modifier (SUMO) gene, SUMO4, in the IDDM5 interval on chromosome 6q25, and presented strong genetic and functional evidence suggesting that SUMO4 is a susceptibility gene for type 1 diabetes mellitus (T1DM). In this article, we will summarize genetic association data suggesting that SUMO4 is consistently associated with T1DM in the Asian populations while the association is more heterogeneous in the Caucasian populations. We will also discuss the possible molecular pathways through which sumoylation may regulate T1DM and autoimmunity. |
| doi_str_mv | 10.1196/annals.1375.039 |
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However, the identification of the specific genes in these intervals presents a formidable challenge due to a number of difficulties associated with genetic mapping and cloning of genes implicated in complex diseases. One of the difficulties is due to the presence of many weak and different susceptibility genes in different patients and populations, a phenomenon known as genetic heterogeneity. In 2004, we reported the cloning of a novel small ubiquitin‐like modifier (SUMO) gene, SUMO4, in the IDDM5 interval on chromosome 6q25, and presented strong genetic and functional evidence suggesting that SUMO4 is a susceptibility gene for type 1 diabetes mellitus (T1DM). In this article, we will summarize genetic association data suggesting that SUMO4 is consistently associated with T1DM in the Asian populations while the association is more heterogeneous in the Caucasian populations. We will also discuss the possible molecular pathways through which sumoylation may regulate T1DM and autoimmunity.</description><subject>antioxidant enzyme</subject><subject>association</subject><subject>Autoimmune Diseases - genetics</subject><subject>autoimmunity</subject><subject>Chromosomes, Human, Pair 6</subject><subject>Diabetes Mellitus, Type 1 - etiology</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>European Continental Ancestry Group - genetics</subject><subject>Forecasting</subject><subject>Genetic Heterogeneity</subject><subject>Genetic Linkage</subject><subject>Genetic Markers</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>IκBα</subject><subject>linkage</subject><subject>Microsatellite Repeats</subject><subject>Mutation</subject><subject>NF-κB</subject><subject>odds ratio (OR)</subject><subject>oxidative stress</subject><subject>pathogenesis</subject><subject>Physical Chromosome Mapping</subject><subject>Reproducibility of Results</subject><subject>risk assessment</subject><subject>Small Ubiquitin-Related Modifier Proteins - genetics</subject><subject>sumoylation</subject><subject>susceptibility</subject><issn>0077-8923</issn><issn>1749-6632</issn><issn>1930-6547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtP3DAURi1EVaa06-4qr9hl8NvxEk1hqKBQaUA8NpaT3CDTTBLihHb-PQ4ZtctZ3c25R590EPpKyZxSo45dXbsqzCnXck642UMzqoVJlOJsH80I0TpJDeMH6FMIz4RQlgr9ER1QTTmRis_QwxJq6H2OXV3gs6HOe99EJT599QXUOeDV0LZN1_v6Ca9uf14L7AJ2-GbTAqb4u3cZ9BAiFXJoe5_5yvcbPEo_ow9l3AZftvcQ3Z6d3izOk8vr5Y_FyWWSSyJNIrLUMVNqUqSpKrksTAG0IKAFk4xlgnFmMq2MoDyXIq6mGR1JTYsSMpPzQ3Q0eduueRkg9Hbt45iqcjU0Q7AqjbwUaifIiGRaS70TpEYYpfloPJ7AvGtC6KC0befXrttYSuzYx0597NjHxj7x49tWPWRrKP7z2yAR4BPwx1ew2eWzVw8nq3dtMn350MPff1-u-23j0MjeXS3t_cXi18UjXVjD3wCcc6p3</recordid><startdate>200610</startdate><enddate>200610</enddate><creator>WANG, CONG-YI</creator><creator>PODOLSKY, ROBERT</creator><creator>SHE, JIN-XIONG</creator><general>Blackwell Publishing Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200610</creationdate><title>Genetic and Functional Evidence Supporting SUMO4 as a Type 1 Diabetes Susceptibility Gene</title><author>WANG, CONG-YI ; PODOLSKY, ROBERT ; SHE, JIN-XIONG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5059-4b8a29f70d886f35d9de1d0e742522b42329b769413c543051b1886f71dfeb9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>antioxidant enzyme</topic><topic>association</topic><topic>Autoimmune Diseases - genetics</topic><topic>autoimmunity</topic><topic>Chromosomes, Human, Pair 6</topic><topic>Diabetes Mellitus, Type 1 - etiology</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>European Continental Ancestry Group - genetics</topic><topic>Forecasting</topic><topic>Genetic Heterogeneity</topic><topic>Genetic Linkage</topic><topic>Genetic Markers</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>IκBα</topic><topic>linkage</topic><topic>Microsatellite Repeats</topic><topic>Mutation</topic><topic>NF-κB</topic><topic>odds ratio (OR)</topic><topic>oxidative stress</topic><topic>pathogenesis</topic><topic>Physical Chromosome Mapping</topic><topic>Reproducibility of Results</topic><topic>risk assessment</topic><topic>Small Ubiquitin-Related Modifier Proteins - genetics</topic><topic>sumoylation</topic><topic>susceptibility</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WANG, CONG-YI</creatorcontrib><creatorcontrib>PODOLSKY, ROBERT</creatorcontrib><creatorcontrib>SHE, JIN-XIONG</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WANG, CONG-YI</au><au>PODOLSKY, ROBERT</au><au>SHE, JIN-XIONG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic and Functional Evidence Supporting SUMO4 as a Type 1 Diabetes Susceptibility Gene</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>2006-10</date><risdate>2006</risdate><volume>1079</volume><issue>1</issue><spage>257</spage><epage>267</epage><pages>257-267</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><eissn>1930-6547</eissn><abstract>: Genomewide linkage analyses since the early 1990s suggested over 20 genomic intervals that may contain susceptibility genes for type 1 diabetes. However, the identification of the specific genes in these intervals presents a formidable challenge due to a number of difficulties associated with genetic mapping and cloning of genes implicated in complex diseases. One of the difficulties is due to the presence of many weak and different susceptibility genes in different patients and populations, a phenomenon known as genetic heterogeneity. In 2004, we reported the cloning of a novel small ubiquitin‐like modifier (SUMO) gene, SUMO4, in the IDDM5 interval on chromosome 6q25, and presented strong genetic and functional evidence suggesting that SUMO4 is a susceptibility gene for type 1 diabetes mellitus (T1DM). In this article, we will summarize genetic association data suggesting that SUMO4 is consistently associated with T1DM in the Asian populations while the association is more heterogeneous in the Caucasian populations. We will also discuss the possible molecular pathways through which sumoylation may regulate T1DM and autoimmunity.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>17130563</pmid><doi>10.1196/annals.1375.039</doi><tpages>11</tpages></addata></record> |
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| subjects | antioxidant enzyme association Autoimmune Diseases - genetics autoimmunity Chromosomes, Human, Pair 6 Diabetes Mellitus, Type 1 - etiology Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - metabolism European Continental Ancestry Group - genetics Forecasting Genetic Heterogeneity Genetic Linkage Genetic Markers Genetic Predisposition to Disease Humans IκBα linkage Microsatellite Repeats Mutation NF-κB odds ratio (OR) oxidative stress pathogenesis Physical Chromosome Mapping Reproducibility of Results risk assessment Small Ubiquitin-Related Modifier Proteins - genetics sumoylation susceptibility |
| title | Genetic and Functional Evidence Supporting SUMO4 as a Type 1 Diabetes Susceptibility Gene |
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