Linkage on Chromosome 3 of Autoimmune Diabetes and Defective Fc Receptor for IgG in NOD Mice
A congenic, non-obese diabetic (NOD) mouse strain that contains a segment of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy-1$^a$ was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the high-affinity Fc re...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 1993-04, Vol.260 (5108), p.695-698 |
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| creator | Prins, Jan-Bas Todd, John A. Rodrigues, Nanda R. Ghosh, Soumitra Hogarth, P. Mark Wicker, Linda S. Gaffney, Erin Podolin, Patricia L. Fischer, Paul A. Sirotina, Anna Peterson, Laurence B. |
| description | A congenic, non-obese diabetic (NOD) mouse strain that contains a segment of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy-1$^a$ was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the high-affinity Fc receptor for immunoglobulin G (IgG), FcγRI. The NOD Fcgr1 allele, which results in a deletion of the cytoplasmic tail, caused a 73 percent reduction in the turnover of cell surface receptor-antibody complexes. The development of congenic strains and the characterization of Mendelian traits that are specific to the disease phenotype demonstrate the feasibility of dissecting the pathophysiology of complex, non-Mendelian diseases. |
| doi_str_mv | 10.1126/science.8480181 |
| format | Article |
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Mark ; Wicker, Linda S. ; Gaffney, Erin ; Podolin, Patricia L. ; Fischer, Paul A. ; Sirotina, Anna ; Peterson, Laurence B.</creator><creatorcontrib>Prins, Jan-Bas ; Todd, John A. ; Rodrigues, Nanda R. ; Ghosh, Soumitra ; Hogarth, P. Mark ; Wicker, Linda S. ; Gaffney, Erin ; Podolin, Patricia L. ; Fischer, Paul A. ; Sirotina, Anna ; Peterson, Laurence B.</creatorcontrib><description>A congenic, non-obese diabetic (NOD) mouse strain that contains a segment of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy-1$^a$ was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the high-affinity Fc receptor for immunoglobulin G (IgG), FcγRI. The NOD Fcgr1 allele, which results in a deletion of the cytoplasmic tail, caused a 73 percent reduction in the turnover of cell surface receptor-antibody complexes. The development of congenic strains and the characterization of Mendelian traits that are specific to the disease phenotype demonstrate the feasibility of dissecting the pathophysiology of complex, non-Mendelian diseases.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.8480181</identifier><identifier>PMID: 8480181</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Society for the Advancement of Science</publisher><subject>Animals ; Autoimmune diseases ; Autoimmune Diseases - genetics ; Base Sequence ; Biological and medical sciences ; Blood cells ; Chromosomes ; Congenic strains ; Crosses, Genetic ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 1 - genetics ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Endocytosis ; Exons ; Female ; Gene Deletion ; Genetic aspects ; Genetic Linkage ; Genetic loci ; Genetic Markers ; Immunoglobulin G - metabolism ; Male ; Medical sciences ; Mice ; Mice, Inbred NOD ; Molecular Sequence Data ; Mutation ; Pathological physiology ; Phenotype ; Phenotypes ; Physiology, Pathological ; Receptors, IgG - genetics ; Receptors, IgG - metabolism ; Type 1 diabetes mellitus</subject><ispartof>Science (American Association for the Advancement of Science), 1993-04, Vol.260 (5108), p.695-698</ispartof><rights>Copyright 1993 American Association for the Advancement of Science</rights><rights>1993 INIST-CNRS</rights><rights>COPYRIGHT 1993 American Association for the Advancement of Science</rights><rights>COPYRIGHT 1993 American Association for the Advancement of Science</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c682t-7153304577e925c7d22ef1c3176f4dbb0448fff5324872efab0586904e66c29e3</citedby><cites>FETCH-LOGICAL-c682t-7153304577e925c7d22ef1c3176f4dbb0448fff5324872efab0586904e66c29e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/2881266$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/2881266$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,2870,2871,27903,27904,57996,58229</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4726662$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8480181$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Prins, Jan-Bas</creatorcontrib><creatorcontrib>Todd, John A.</creatorcontrib><creatorcontrib>Rodrigues, Nanda R.</creatorcontrib><creatorcontrib>Ghosh, Soumitra</creatorcontrib><creatorcontrib>Hogarth, P. Mark</creatorcontrib><creatorcontrib>Wicker, Linda S.</creatorcontrib><creatorcontrib>Gaffney, Erin</creatorcontrib><creatorcontrib>Podolin, Patricia L.</creatorcontrib><creatorcontrib>Fischer, Paul A.</creatorcontrib><creatorcontrib>Sirotina, Anna</creatorcontrib><creatorcontrib>Peterson, Laurence B.</creatorcontrib><title>Linkage on Chromosome 3 of Autoimmune Diabetes and Defective Fc Receptor for IgG in NOD Mice</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>A congenic, non-obese diabetic (NOD) mouse strain that contains a segment of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy-1$^a$ was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the high-affinity Fc receptor for immunoglobulin G (IgG), FcγRI. The NOD Fcgr1 allele, which results in a deletion of the cytoplasmic tail, caused a 73 percent reduction in the turnover of cell surface receptor-antibody complexes. The development of congenic strains and the characterization of Mendelian traits that are specific to the disease phenotype demonstrate the feasibility of dissecting the pathophysiology of complex, non-Mendelian diseases.</description><subject>Animals</subject><subject>Autoimmune diseases</subject><subject>Autoimmune Diseases - genetics</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Blood cells</subject><subject>Chromosomes</subject><subject>Congenic strains</subject><subject>Crosses, Genetic</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Endocytosis</subject><subject>Exons</subject><subject>Female</subject><subject>Gene Deletion</subject><subject>Genetic aspects</subject><subject>Genetic Linkage</subject><subject>Genetic loci</subject><subject>Genetic Markers</subject><subject>Immunoglobulin G - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Pathological physiology</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Physiology, Pathological</subject><subject>Receptors, IgG - genetics</subject><subject>Receptors, IgG - metabolism</subject><subject>Type 1 diabetes mellitus</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0s1r2zAYBnAzVrqs23mXDXQoY4e61Ycty8csWdNA1sC-TgMhK688dbaUWfbY_vupxGQEcghGGPT8JB3eJ0leEXxNCOU3QVtwGq5FJjAR5EkyIbjM05Ji9jSZYMx4KnCRP0ueh_CAccxKdp6cj3ySfF9Z91PVgLxDsx-db33wLSCGvEHTofe2bQcHaG5VBT0EpNwGzcGA7u1vQLcafQIN2953yMS1rBfIOnS_nqOPVsOL5MyoJsDL8X-RfL398GV2l67Wi-Vsuko1F7RPC5IzhrO8KKCkuS42lIIhmpGCm2xTVTjLhDEmZzQTRYxUhXPBS5wB55qWwC6St7t7t53_NUDoZWuDhqZRDvwQZJEXmBFKI7zawVo1IK0zvu-UrsFBpxrvwNi4PSVM5FQQEnl6hMdvA63Vx_y7Ax9JD3_6Wg0hyOXn-5Pp-tvJ9P3iVCoWqwN6dYxq3zRQg4zzma0P-M2O686H0IGR2862qvsrCZaPTZRjE-VYrXjizTiUoWphs_f_88sxV0GrxnTKaRv2LCso5_xxZK937CHElu1jKkR8lLN_Xk_pQw</recordid><startdate>19930430</startdate><enddate>19930430</enddate><creator>Prins, Jan-Bas</creator><creator>Todd, John A.</creator><creator>Rodrigues, Nanda R.</creator><creator>Ghosh, Soumitra</creator><creator>Hogarth, P. Mark</creator><creator>Wicker, Linda S.</creator><creator>Gaffney, Erin</creator><creator>Podolin, Patricia L.</creator><creator>Fischer, Paul A.</creator><creator>Sirotina, Anna</creator><creator>Peterson, Laurence B.</creator><general>American Society for the Advancement of Science</general><general>American Association for the Advancement of Science</general><scope>IQODW</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>8GL</scope><scope>IBG</scope><scope>IOV</scope><scope>ISN</scope><scope>7X8</scope></search><sort><creationdate>19930430</creationdate><title>Linkage on Chromosome 3 of Autoimmune Diabetes and Defective Fc Receptor for IgG in NOD Mice</title><author>Prins, Jan-Bas ; Todd, John A. ; Rodrigues, Nanda R. ; Ghosh, Soumitra ; Hogarth, P. Mark ; Wicker, Linda S. ; Gaffney, Erin ; Podolin, Patricia L. ; Fischer, Paul A. ; Sirotina, Anna ; Peterson, Laurence B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c682t-7153304577e925c7d22ef1c3176f4dbb0448fff5324872efab0586904e66c29e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Autoimmune diseases</topic><topic>Autoimmune Diseases - genetics</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Blood cells</topic><topic>Chromosomes</topic><topic>Congenic strains</topic><topic>Crosses, Genetic</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Endocytosis</topic><topic>Exons</topic><topic>Female</topic><topic>Gene Deletion</topic><topic>Genetic aspects</topic><topic>Genetic Linkage</topic><topic>Genetic loci</topic><topic>Genetic Markers</topic><topic>Immunoglobulin G - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Molecular Sequence Data</topic><topic>Mutation</topic><topic>Pathological physiology</topic><topic>Phenotype</topic><topic>Phenotypes</topic><topic>Physiology, Pathological</topic><topic>Receptors, IgG - genetics</topic><topic>Receptors, IgG - metabolism</topic><topic>Type 1 diabetes mellitus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Prins, Jan-Bas</creatorcontrib><creatorcontrib>Todd, John A.</creatorcontrib><creatorcontrib>Rodrigues, Nanda R.</creatorcontrib><creatorcontrib>Ghosh, Soumitra</creatorcontrib><creatorcontrib>Hogarth, P. Mark</creatorcontrib><creatorcontrib>Wicker, Linda S.</creatorcontrib><creatorcontrib>Gaffney, Erin</creatorcontrib><creatorcontrib>Podolin, Patricia L.</creatorcontrib><creatorcontrib>Fischer, Paul A.</creatorcontrib><creatorcontrib>Sirotina, Anna</creatorcontrib><creatorcontrib>Peterson, Laurence B.</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>Gale In Context: High School</collection><collection>Gale In Context: Biography</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Canada</collection><collection>MEDLINE - Academic</collection><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Prins, Jan-Bas</au><au>Todd, John A.</au><au>Rodrigues, Nanda R.</au><au>Ghosh, Soumitra</au><au>Hogarth, P. Mark</au><au>Wicker, Linda S.</au><au>Gaffney, Erin</au><au>Podolin, Patricia L.</au><au>Fischer, Paul A.</au><au>Sirotina, Anna</au><au>Peterson, Laurence B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Linkage on Chromosome 3 of Autoimmune Diabetes and Defective Fc Receptor for IgG in NOD Mice</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>1993-04-30</date><risdate>1993</risdate><volume>260</volume><issue>5108</issue><spage>695</spage><epage>698</epage><pages>695-698</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><abstract>A congenic, non-obese diabetic (NOD) mouse strain that contains a segment of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy-1$^a$ was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the high-affinity Fc receptor for immunoglobulin G (IgG), FcγRI. The NOD Fcgr1 allele, which results in a deletion of the cytoplasmic tail, caused a 73 percent reduction in the turnover of cell surface receptor-antibody complexes. The development of congenic strains and the characterization of Mendelian traits that are specific to the disease phenotype demonstrate the feasibility of dissecting the pathophysiology of complex, non-Mendelian diseases.</abstract><cop>Washington, DC</cop><pub>American Society for the Advancement of Science</pub><pmid>8480181</pmid><doi>10.1126/science.8480181</doi><tpages>4</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0036-8075 |
| ispartof | Science (American Association for the Advancement of Science), 1993-04, Vol.260 (5108), p.695-698 |
| issn | 0036-8075 1095-9203 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_75703122 |
| source | MEDLINE; American Association for the Advancement of Science; Jstor Complete Legacy |
| subjects | Animals Autoimmune diseases Autoimmune Diseases - genetics Base Sequence Biological and medical sciences Blood cells Chromosomes Congenic strains Crosses, Genetic Diabetes Diabetes mellitus Diabetes Mellitus, Type 1 - genetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies Endocytosis Exons Female Gene Deletion Genetic aspects Genetic Linkage Genetic loci Genetic Markers Immunoglobulin G - metabolism Male Medical sciences Mice Mice, Inbred NOD Molecular Sequence Data Mutation Pathological physiology Phenotype Phenotypes Physiology, Pathological Receptors, IgG - genetics Receptors, IgG - metabolism Type 1 diabetes mellitus |
| title | Linkage on Chromosome 3 of Autoimmune Diabetes and Defective Fc Receptor for IgG in NOD Mice |
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