Complement C4 and heat shock protein 70 (HSP70) genotypes and type I diabetes mellitus
Type I diabetes is strongly associated with the major histocompatibility complex (MHC) class II region (DR and DQ loci), and to a lesser extent the class III region (complement C4 loci). Restriction fragment length polymorphism analysis was employed to investigate the C4 and heat shock protein 70 (H...
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| Veröffentlicht in: | Immunogenetics (New York) 1990-12, Vol.32 (6), p.427-430 |
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| container_title | Immunogenetics (New York) |
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| creator | CAPLEN, N. J PATEL, A MILLWARD, A DUNCAN CAMPBELL, R RATANACHAIYAVONG, S WONG, F. S DEMAINE, A. G |
| description | Type I diabetes is strongly associated with the major histocompatibility complex (MHC) class II region (DR and DQ loci), and to a lesser extent the class III region (complement C4 loci). Restriction fragment length polymorphism analysis was employed to investigate the C4 and heat shock protein 70 (HSP70) loci of 176 patients with type I diabetes and 92 healthy controls. In the patient population there was an excess of deletions of the C4A locus (48.5% vs 22.1%, P less than 0.0005). The HSP70 probe in conjunction with the restriction endonuclease Pst I detects two alleles of 9 or 8.5 kilobases (kb). The 8.5 kb allele was significantly increased in the patient group compared to healthy controls (0.569 vs 0.353, respectively, P less than 0.0005). Furthermore, a C4A deletion nearly always occurred with the 8.5 kb HSP70 allele, suggesting that it may be a marker of the HLA-A1,B8,C4A deletion, DR3 extended haplotype. |
| doi_str_mv | 10.1007/BF00241637 |
| format | Article |
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J ; PATEL, A ; MILLWARD, A ; DUNCAN CAMPBELL, R ; RATANACHAIYAVONG, S ; WONG, F. S ; DEMAINE, A. G</creator><creatorcontrib>CAPLEN, N. J ; PATEL, A ; MILLWARD, A ; DUNCAN CAMPBELL, R ; RATANACHAIYAVONG, S ; WONG, F. S ; DEMAINE, A. G</creatorcontrib><description>Type I diabetes is strongly associated with the major histocompatibility complex (MHC) class II region (DR and DQ loci), and to a lesser extent the class III region (complement C4 loci). Restriction fragment length polymorphism analysis was employed to investigate the C4 and heat shock protein 70 (HSP70) loci of 176 patients with type I diabetes and 92 healthy controls. In the patient population there was an excess of deletions of the C4A locus (48.5% vs 22.1%, P less than 0.0005). The HSP70 probe in conjunction with the restriction endonuclease Pst I detects two alleles of 9 or 8.5 kilobases (kb). The 8.5 kb allele was significantly increased in the patient group compared to healthy controls (0.569 vs 0.353, respectively, P less than 0.0005). Furthermore, a C4A deletion nearly always occurred with the 8.5 kb HSP70 allele, suggesting that it may be a marker of the HLA-A1,B8,C4A deletion, DR3 extended haplotype.</description><identifier>ISSN: 0093-7711</identifier><identifier>EISSN: 1432-1211</identifier><identifier>DOI: 10.1007/BF00241637</identifier><identifier>PMID: 2272664</identifier><identifier>CODEN: IMNGBK</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Biological and medical sciences ; Complement C4 - genetics ; Diabetes Mellitus, Type 1 - genetics ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Gene Frequency ; Genotype ; Heat-Shock Proteins - genetics ; HLA Antigens - genetics ; HLA-DR Antigens - genetics ; Humans ; Medical sciences</subject><ispartof>Immunogenetics (New York), 1990-12, Vol.32 (6), p.427-430</ispartof><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c312t-c9a4c7723b3cfd36632bb36d9c9af9d2d03c18ceee6d219a0938aad47a8e839b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19637896$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2272664$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CAPLEN, N. J</creatorcontrib><creatorcontrib>PATEL, A</creatorcontrib><creatorcontrib>MILLWARD, A</creatorcontrib><creatorcontrib>DUNCAN CAMPBELL, R</creatorcontrib><creatorcontrib>RATANACHAIYAVONG, S</creatorcontrib><creatorcontrib>WONG, F. S</creatorcontrib><creatorcontrib>DEMAINE, A. G</creatorcontrib><title>Complement C4 and heat shock protein 70 (HSP70) genotypes and type I diabetes mellitus</title><title>Immunogenetics (New York)</title><addtitle>Immunogenetics</addtitle><description>Type I diabetes is strongly associated with the major histocompatibility complex (MHC) class II region (DR and DQ loci), and to a lesser extent the class III region (complement C4 loci). Restriction fragment length polymorphism analysis was employed to investigate the C4 and heat shock protein 70 (HSP70) loci of 176 patients with type I diabetes and 92 healthy controls. In the patient population there was an excess of deletions of the C4A locus (48.5% vs 22.1%, P less than 0.0005). The HSP70 probe in conjunction with the restriction endonuclease Pst I detects two alleles of 9 or 8.5 kilobases (kb). The 8.5 kb allele was significantly increased in the patient group compared to healthy controls (0.569 vs 0.353, respectively, P less than 0.0005). Furthermore, a C4A deletion nearly always occurred with the 8.5 kb HSP70 allele, suggesting that it may be a marker of the HLA-A1,B8,C4A deletion, DR3 extended haplotype.</description><subject>Biological and medical sciences</subject><subject>Complement C4 - genetics</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Gene Frequency</subject><subject>Genotype</subject><subject>Heat-Shock Proteins - genetics</subject><subject>HLA Antigens - genetics</subject><subject>HLA-DR Antigens - genetics</subject><subject>Humans</subject><subject>Medical sciences</subject><issn>0093-7711</issn><issn>1432-1211</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtLAzEQxoMotVYv3oVcFBVW81iTzVEXawsFBR_XJZvM2tV9ucke-t-b2mIvM8N8Pz5mPoROKbmhhMjbhykhLKaCyz00pjFnEWWU7qMxIYpHUlJ6iI6c-yKE3ikmRmjEmGRCxGP0kbZ1V0ENjcdpjHVj8RK0x27Zmm_c9a2HssGS4MvZ64skV_gTmtavOnB_7HrCc2xLnYMPuxqqqvSDO0YHha4cnGz7BL1PH9_SWbR4fpqn94vIcMp8ZJSOjZSM59wUlgvBWZ5zYVUQCmWZJdzQxACAsIwqHd5JtLax1AkkXOV8gi42vuHSnwGcz-rSmXCEbqAdXJYQRnlMVQCvN6DpW-d6KLKuL2vdrzJKsnWI2S7EAJ9tXYe8BvuPblML-vlW187oquh1Y0q3c1TBJAnlFwVKdzk</recordid><startdate>19901201</startdate><enddate>19901201</enddate><creator>CAPLEN, N. 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G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c312t-c9a4c7723b3cfd36632bb36d9c9af9d2d03c18ceee6d219a0938aad47a8e839b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Biological and medical sciences</topic><topic>Complement C4 - genetics</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Gene Frequency</topic><topic>Genotype</topic><topic>Heat-Shock Proteins - genetics</topic><topic>HLA Antigens - genetics</topic><topic>HLA-DR Antigens - genetics</topic><topic>Humans</topic><topic>Medical sciences</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CAPLEN, N. J</creatorcontrib><creatorcontrib>PATEL, A</creatorcontrib><creatorcontrib>MILLWARD, A</creatorcontrib><creatorcontrib>DUNCAN CAMPBELL, R</creatorcontrib><creatorcontrib>RATANACHAIYAVONG, S</creatorcontrib><creatorcontrib>WONG, F. S</creatorcontrib><creatorcontrib>DEMAINE, A. G</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Immunogenetics (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CAPLEN, N. J</au><au>PATEL, A</au><au>MILLWARD, A</au><au>DUNCAN CAMPBELL, R</au><au>RATANACHAIYAVONG, S</au><au>WONG, F. S</au><au>DEMAINE, A. G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Complement C4 and heat shock protein 70 (HSP70) genotypes and type I diabetes mellitus</atitle><jtitle>Immunogenetics (New York)</jtitle><addtitle>Immunogenetics</addtitle><date>1990-12-01</date><risdate>1990</risdate><volume>32</volume><issue>6</issue><spage>427</spage><epage>430</epage><pages>427-430</pages><issn>0093-7711</issn><eissn>1432-1211</eissn><coden>IMNGBK</coden><abstract>Type I diabetes is strongly associated with the major histocompatibility complex (MHC) class II region (DR and DQ loci), and to a lesser extent the class III region (complement C4 loci). Restriction fragment length polymorphism analysis was employed to investigate the C4 and heat shock protein 70 (HSP70) loci of 176 patients with type I diabetes and 92 healthy controls. In the patient population there was an excess of deletions of the C4A locus (48.5% vs 22.1%, P less than 0.0005). The HSP70 probe in conjunction with the restriction endonuclease Pst I detects two alleles of 9 or 8.5 kilobases (kb). The 8.5 kb allele was significantly increased in the patient group compared to healthy controls (0.569 vs 0.353, respectively, P less than 0.0005). Furthermore, a C4A deletion nearly always occurred with the 8.5 kb HSP70 allele, suggesting that it may be a marker of the HLA-A1,B8,C4A deletion, DR3 extended haplotype.</abstract><cop>Heidelberg</cop><cop>Berlin</cop><pub>Springer</pub><pmid>2272664</pmid><doi>10.1007/BF00241637</doi><tpages>4</tpages></addata></record> |
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| subjects | Biological and medical sciences Complement C4 - genetics Diabetes Mellitus, Type 1 - genetics Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Gene Frequency Genotype Heat-Shock Proteins - genetics HLA Antigens - genetics HLA-DR Antigens - genetics Humans Medical sciences |
| title | Complement C4 and heat shock protein 70 (HSP70) genotypes and type I diabetes mellitus |
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