Insulin Transactivator MafA Regulates Intrathymic Expression of Insulin and Affects Susceptibility to Type 1 Diabetes
Tissue-specific self-antigens are ectopically expressed within the thymus and play an important role in the induction of central tolerance. Insulin is expressed in both pancreatic islets and the thymus and is considered to be the primary antigen for type 1 diabetes. Here, we report the role of the i...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2010-10, Vol.59 (10), p.2579-2587 |
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| creator | NOSO, Shinsuke KATAOKA, Kohsuke IKEGAMI, Hiroshi KAWABATA, Yumiko BABAYA, Naru HIROMINE, Yoshihisa YAMAJI, Kaori FUJISAWA, Tomomi ARAMATA, Shinsaku KUDO, Takashi TAKAHASHI, Satoru |
| description | Tissue-specific self-antigens are ectopically expressed within the thymus and play an important role in the induction of central tolerance. Insulin is expressed in both pancreatic islets and the thymus and is considered to be the primary antigen for type 1 diabetes. Here, we report the role of the insulin transactivator MafA in the expression of insulin in the thymus and susceptibility to type 1 diabetes.
The expression profiles of transcriptional factors (Pdx1, NeuroD, Mafa, and Aire) in pancreatic islets and the thymus were examined in nonobese diabetic (NOD) and control mice. Thymic Ins2 expression and serum autoantibodies were examined in Mafa knockout mice. Luciferase reporter assay was performed for newly identified polymorphisms of mouse Mafa and human MAFA. A case-control study was applied for human MAFA polymorphisms.
Mafa, Ins2, and Aire expression was detected in the thymus. Mafa expression was lower in NOD thymus than in the control and was correlated with Ins2 expression. Targeted disruption of MafA reduced thymic Ins2 expression and induced autoantibodies against pancreatic islets. Functional polymorphisms of MafA were newly identified in NOD mice and humans, and polymorphisms of human MAFA were associated with susceptibility to type 1 diabetes but not to autoimmune thyroid disease.
These data indicate that functional polymorphisms of MafA are associated with reduced expression of insulin in the thymus and susceptibility to type 1 diabetes in the NOD mouse as well as human type 1 diabetes. |
| doi_str_mv | 10.2337/db10-0476 |
| format | Article |
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The expression profiles of transcriptional factors (Pdx1, NeuroD, Mafa, and Aire) in pancreatic islets and the thymus were examined in nonobese diabetic (NOD) and control mice. Thymic Ins2 expression and serum autoantibodies were examined in Mafa knockout mice. Luciferase reporter assay was performed for newly identified polymorphisms of mouse Mafa and human MAFA. A case-control study was applied for human MAFA polymorphisms.
Mafa, Ins2, and Aire expression was detected in the thymus. Mafa expression was lower in NOD thymus than in the control and was correlated with Ins2 expression. Targeted disruption of MafA reduced thymic Ins2 expression and induced autoantibodies against pancreatic islets. Functional polymorphisms of MafA were newly identified in NOD mice and humans, and polymorphisms of human MAFA were associated with susceptibility to type 1 diabetes but not to autoimmune thyroid disease.
These data indicate that functional polymorphisms of MafA are associated with reduced expression of insulin in the thymus and susceptibility to type 1 diabetes in the NOD mouse as well as human type 1 diabetes.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/db10-0476</identifier><identifier>PMID: 20682694</identifier><identifier>CODEN: DIAEAZ</identifier><language>eng</language><publisher>Alexandria, VA: American Diabetes Association</publisher><subject>AIRE Protein ; Animals ; Antibodies ; Antigens ; Autoimmune diseases ; Biological and medical sciences ; Development and progression ; Diabetes ; Diabetes Mellitus, Type 1 - genetics ; Diabetes. Impaired glucose tolerance ; Disease ; DNA-Binding Proteins - genetics ; Dosage and administration ; Drug therapy ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Genes ; Genetic Predisposition to Disease ; Genetic regulation ; Genetic susceptibility ; Humans ; Immunohistochemistry ; Immunology and Transplantation ; Insulin ; Insulin - genetics ; Islets of Langerhans - cytology ; Islets of Langerhans - physiology ; Laboratories ; Maf Transcription Factors, Large - deficiency ; Maf Transcription Factors, Large - genetics ; Maf Transcription Factors, Large - physiology ; Male ; Medical sciences ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Promoter Regions, Genetic ; Regulation ; Research design ; Reverse Transcriptase Polymerase Chain Reaction ; Risk factors ; Thymus gland ; Thymus Gland - physiology ; Thyroid gland ; Transcription Factors - genetics ; Transcription, Genetic ; Type 1 diabetes</subject><ispartof>Diabetes (New York, N.Y.), 2010-10, Vol.59 (10), p.2579-2587</ispartof><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2010 American Diabetes Association</rights><rights>Copyright American Diabetes Association Oct 2010</rights><rights>2010 by the American Diabetes Association. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c674t-708c238fdbf299f474c3642f4f86624b33c42c9209cba88962d6aceabef8d7e03</citedby><cites>FETCH-LOGICAL-c674t-708c238fdbf299f474c3642f4f86624b33c42c9209cba88962d6aceabef8d7e03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279543/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279543/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23327779$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20682694$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NOSO, Shinsuke</creatorcontrib><creatorcontrib>KATAOKA, Kohsuke</creatorcontrib><creatorcontrib>IKEGAMI, Hiroshi</creatorcontrib><creatorcontrib>KAWABATA, Yumiko</creatorcontrib><creatorcontrib>BABAYA, Naru</creatorcontrib><creatorcontrib>HIROMINE, Yoshihisa</creatorcontrib><creatorcontrib>YAMAJI, Kaori</creatorcontrib><creatorcontrib>FUJISAWA, Tomomi</creatorcontrib><creatorcontrib>ARAMATA, Shinsaku</creatorcontrib><creatorcontrib>KUDO, Takashi</creatorcontrib><creatorcontrib>TAKAHASHI, Satoru</creatorcontrib><title>Insulin Transactivator MafA Regulates Intrathymic Expression of Insulin and Affects Susceptibility to Type 1 Diabetes</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>Tissue-specific self-antigens are ectopically expressed within the thymus and play an important role in the induction of central tolerance. Insulin is expressed in both pancreatic islets and the thymus and is considered to be the primary antigen for type 1 diabetes. Here, we report the role of the insulin transactivator MafA in the expression of insulin in the thymus and susceptibility to type 1 diabetes.
The expression profiles of transcriptional factors (Pdx1, NeuroD, Mafa, and Aire) in pancreatic islets and the thymus were examined in nonobese diabetic (NOD) and control mice. Thymic Ins2 expression and serum autoantibodies were examined in Mafa knockout mice. Luciferase reporter assay was performed for newly identified polymorphisms of mouse Mafa and human MAFA. A case-control study was applied for human MAFA polymorphisms.
Mafa, Ins2, and Aire expression was detected in the thymus. Mafa expression was lower in NOD thymus than in the control and was correlated with Ins2 expression. Targeted disruption of MafA reduced thymic Ins2 expression and induced autoantibodies against pancreatic islets. Functional polymorphisms of MafA were newly identified in NOD mice and humans, and polymorphisms of human MAFA were associated with susceptibility to type 1 diabetes but not to autoimmune thyroid disease.
These data indicate that functional polymorphisms of MafA are associated with reduced expression of insulin in the thymus and susceptibility to type 1 diabetes in the NOD mouse as well as human type 1 diabetes.</description><subject>AIRE Protein</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Autoimmune diseases</subject><subject>Biological and medical sciences</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Disease</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic regulation</subject><subject>Genetic susceptibility</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Immunology and Transplantation</subject><subject>Insulin</subject><subject>Insulin - genetics</subject><subject>Islets of Langerhans - cytology</subject><subject>Islets of Langerhans - physiology</subject><subject>Laboratories</subject><subject>Maf Transcription Factors, Large - deficiency</subject><subject>Maf Transcription Factors, Large - genetics</subject><subject>Maf Transcription Factors, Large - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, Knockout</subject><subject>Promoter Regions, Genetic</subject><subject>Regulation</subject><subject>Research design</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Risk factors</subject><subject>Thymus gland</subject><subject>Thymus Gland - physiology</subject><subject>Thyroid gland</subject><subject>Transcription Factors - genetics</subject><subject>Transcription, Genetic</subject><subject>Type 1 diabetes</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kl2LEzEUhgdR3Lp64R-QoIh4MWsmSZPJjVDquhYqC1rBu5DJnHSzTJM6ySzbf2-G7a5WiuQikDznPV9vUbys8BmhVHxomwqXmAn-qJhUksqSEvHzcTHBuCJlJaQ4KZ7FeI0x5vk8LU4I5jXhkk2KYeHj0DmPVr32UZvkbnQKPfqq7Qx9g_XQ6QQRLXzqdbrabZxB57fbHmJ0waNg0X289i2aWQsmRfR9iAa2yTWuc2mHUkCr3RZQhT453UDWe148sbqL8GJ_nxY_Pp-v5l_K5eXFYj5bloYLlkqBa0NobdvGEiktE8xQzohltuacsIZSw4iRBEvT6LqWnLRcG8g5bN0KwPS0-Hinux2aDbQGxjY6te3dRvc7FbRThz_eXal1uFF5gHLKaBZ4txfow68BYlIbl3vrOu0hDFGJ6VTyWtIx1et_yOsw9D53p2pSSSG55Bl6cwetdQfKeRtyVjNKqhlhmNViKqaZKo9Qa_CQSwwerMvPB_zZET6fFvK-jga8PwjITILbtNZDzNVeLP9XzJ41oetgDSqva355VNv0IcYe7MO0K6xGt6rRrWp0a2Zf_b2eB_Lenhl4uwd0NLqz2aPGxT8czXsSQtLfPMjv4A</recordid><startdate>20101001</startdate><enddate>20101001</enddate><creator>NOSO, Shinsuke</creator><creator>KATAOKA, Kohsuke</creator><creator>IKEGAMI, Hiroshi</creator><creator>KAWABATA, Yumiko</creator><creator>BABAYA, Naru</creator><creator>HIROMINE, Yoshihisa</creator><creator>YAMAJI, Kaori</creator><creator>FUJISAWA, Tomomi</creator><creator>ARAMATA, Shinsaku</creator><creator>KUDO, Takashi</creator><creator>TAKAHASHI, Satoru</creator><general>American Diabetes Association</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20101001</creationdate><title>Insulin Transactivator MafA Regulates Intrathymic Expression of Insulin and Affects Susceptibility to Type 1 Diabetes</title><author>NOSO, Shinsuke ; KATAOKA, Kohsuke ; IKEGAMI, Hiroshi ; KAWABATA, Yumiko ; BABAYA, Naru ; HIROMINE, Yoshihisa ; YAMAJI, Kaori ; FUJISAWA, Tomomi ; ARAMATA, Shinsaku ; KUDO, Takashi ; TAKAHASHI, Satoru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c674t-708c238fdbf299f474c3642f4f86624b33c42c9209cba88962d6aceabef8d7e03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>AIRE Protein</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antigens</topic><topic>Autoimmune diseases</topic><topic>Biological and medical sciences</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Disease</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Genes</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic regulation</topic><topic>Genetic susceptibility</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Immunology and Transplantation</topic><topic>Insulin</topic><topic>Insulin - genetics</topic><topic>Islets of Langerhans - cytology</topic><topic>Islets of Langerhans - physiology</topic><topic>Laboratories</topic><topic>Maf Transcription Factors, Large - deficiency</topic><topic>Maf Transcription Factors, Large - genetics</topic><topic>Maf Transcription Factors, Large - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, Knockout</topic><topic>Promoter Regions, Genetic</topic><topic>Regulation</topic><topic>Research design</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Risk factors</topic><topic>Thymus gland</topic><topic>Thymus Gland - physiology</topic><topic>Thyroid gland</topic><topic>Transcription Factors - genetics</topic><topic>Transcription, Genetic</topic><topic>Type 1 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NOSO, Shinsuke</creatorcontrib><creatorcontrib>KATAOKA, Kohsuke</creatorcontrib><creatorcontrib>IKEGAMI, Hiroshi</creatorcontrib><creatorcontrib>KAWABATA, Yumiko</creatorcontrib><creatorcontrib>BABAYA, Naru</creatorcontrib><creatorcontrib>HIROMINE, Yoshihisa</creatorcontrib><creatorcontrib>YAMAJI, Kaori</creatorcontrib><creatorcontrib>FUJISAWA, Tomomi</creatorcontrib><creatorcontrib>ARAMATA, Shinsaku</creatorcontrib><creatorcontrib>KUDO, Takashi</creatorcontrib><creatorcontrib>TAKAHASHI, Satoru</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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Diabetes (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NOSO, Shinsuke</au><au>KATAOKA, Kohsuke</au><au>IKEGAMI, Hiroshi</au><au>KAWABATA, Yumiko</au><au>BABAYA, Naru</au><au>HIROMINE, Yoshihisa</au><au>YAMAJI, Kaori</au><au>FUJISAWA, Tomomi</au><au>ARAMATA, Shinsaku</au><au>KUDO, Takashi</au><au>TAKAHASHI, Satoru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insulin Transactivator MafA Regulates Intrathymic Expression of Insulin and Affects Susceptibility to Type 1 Diabetes</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><addtitle>Diabetes</addtitle><date>2010-10-01</date><risdate>2010</risdate><volume>59</volume><issue>10</issue><spage>2579</spage><epage>2587</epage><pages>2579-2587</pages><issn>0012-1797</issn><eissn>1939-327X</eissn><coden>DIAEAZ</coden><abstract>Tissue-specific self-antigens are ectopically expressed within the thymus and play an important role in the induction of central tolerance. Insulin is expressed in both pancreatic islets and the thymus and is considered to be the primary antigen for type 1 diabetes. Here, we report the role of the insulin transactivator MafA in the expression of insulin in the thymus and susceptibility to type 1 diabetes.
The expression profiles of transcriptional factors (Pdx1, NeuroD, Mafa, and Aire) in pancreatic islets and the thymus were examined in nonobese diabetic (NOD) and control mice. Thymic Ins2 expression and serum autoantibodies were examined in Mafa knockout mice. Luciferase reporter assay was performed for newly identified polymorphisms of mouse Mafa and human MAFA. A case-control study was applied for human MAFA polymorphisms.
Mafa, Ins2, and Aire expression was detected in the thymus. Mafa expression was lower in NOD thymus than in the control and was correlated with Ins2 expression. Targeted disruption of MafA reduced thymic Ins2 expression and induced autoantibodies against pancreatic islets. Functional polymorphisms of MafA were newly identified in NOD mice and humans, and polymorphisms of human MAFA were associated with susceptibility to type 1 diabetes but not to autoimmune thyroid disease.
These data indicate that functional polymorphisms of MafA are associated with reduced expression of insulin in the thymus and susceptibility to type 1 diabetes in the NOD mouse as well as human type 1 diabetes.</abstract><cop>Alexandria, VA</cop><pub>American Diabetes Association</pub><pmid>20682694</pmid><doi>10.2337/db10-0476</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0012-1797 |
| ispartof | Diabetes (New York, N.Y.), 2010-10, Vol.59 (10), p.2579-2587 |
| issn | 0012-1797 1939-327X |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3279543 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | AIRE Protein Animals Antibodies Antigens Autoimmune diseases Biological and medical sciences Development and progression Diabetes Diabetes Mellitus, Type 1 - genetics Diabetes. Impaired glucose tolerance Disease DNA-Binding Proteins - genetics Dosage and administration Drug therapy Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gene Expression Profiling Gene Expression Regulation Genes Genetic Predisposition to Disease Genetic regulation Genetic susceptibility Humans Immunohistochemistry Immunology and Transplantation Insulin Insulin - genetics Islets of Langerhans - cytology Islets of Langerhans - physiology Laboratories Maf Transcription Factors, Large - deficiency Maf Transcription Factors, Large - genetics Maf Transcription Factors, Large - physiology Male Medical sciences Mice Mice, Inbred NOD Mice, Knockout Promoter Regions, Genetic Regulation Research design Reverse Transcriptase Polymerase Chain Reaction Risk factors Thymus gland Thymus Gland - physiology Thyroid gland Transcription Factors - genetics Transcription, Genetic Type 1 diabetes |
| title | Insulin Transactivator MafA Regulates Intrathymic Expression of Insulin and Affects Susceptibility to Type 1 Diabetes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T16%3A31%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Insulin%20Transactivator%20MafA%20Regulates%20Intrathymic%20Expression%20of%20Insulin%20and%20Affects%20Susceptibility%20to%20Type%201%20Diabetes&rft.jtitle=Diabetes%20(New%20York,%20N.Y.)&rft.au=NOSO,%20Shinsuke&rft.date=2010-10-01&rft.volume=59&rft.issue=10&rft.spage=2579&rft.epage=2587&rft.pages=2579-2587&rft.issn=0012-1797&rft.eissn=1939-327X&rft.coden=DIAEAZ&rft_id=info:doi/10.2337/db10-0476&rft_dat=%3Cgale_pubme%3EA240487575%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=821979696&rft_id=info:pmid/20682694&rft_galeid=A240487575&rfr_iscdi=true |