RDF of MGI data
表現型アノテーション
increased susceptibility to autoimmune diabetes_Tgfbr2<tm1.2Hlm>/Tgfbr2<tm1.2Hlm>,Tnfrsf4<tm2(cre)Nik>/Tnfrsf4<+>,Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/0
http://metadb.riken.jp/0004803I129C57BL6NODSJLTgfbr2tm12HlmTgfbr2tm12HlmTnfrsf4tm2creNikTnfrsf4TgTcraBDC25TcrbBDC251Doi0Tgfbr2tm12HlmTgTcraBDC25TcrbBDC251DoiTnfrsf4tm2creNikTnfrsf4
increased susceptibility to autoimmune diabetes_Tgfbr2<tm1.2Hlm>/Tgfbr2<tm1.2Hlm>,Tnfrsf4<tm2(cre)Nik>/Tnfrsf4<+>,Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/0(表現型アノテーション)
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increased susceptibility to autoimmune diabetes_Tgfbr2<tm1.2Hlm>/Tgfbr2<tm1.2Hlm>,Tnfrsf4<tm2(cre)Nik>/Tnfrsf4<+>,Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/0
表現型アノテーション
MGI marker
http://metadb.riken.jp/db/mgi_rdf/variant_of
tumor necrosis factor receptor superfamily, member 4
http://metadb.riken.jp/db/mgi_rdf/MGI:104512
transforming growth factor, beta receptor II
http://metadb.riken.jp/db/mgi_rdf/MGI:98729
transgene insertion 1, Christophe Benoist
http://metadb.riken.jp/db/mgi_rdf/MGI:3612117
遺伝子型
http://metadb.riken.jp/db/mgi_rdf/allele_composition
Tgfbr2<tm1.2Hlm>/Tgfbr2<tm1.2Hlm>,Tnfrsf4<tm2(cre)Nik>/Tnfrsf4<+>,Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/0
アレルシンボル
http://metadb.riken.jp/db/mgi_rdf/allele_symbol
Tgfbr2<tm1.2Hlm>|Tg(TcraBDC2.5,TcrbBDC2.5)1Doi|Tnfrsf4<tm2(cre)Nik>|Tnfrsf4<+>
遺伝的背景
http://metadb.riken.jp/db/mgi_rdf/genetic_background
involves: 129 * C57BL/6 * NOD * SJL
MP annotation
http://metadb.riken.jp/db/bioresource_schema/brs_indicatesPhenotype
increased susceptibility to autoimmune diabetes
http://purl.obolibrary.org/obo/MP_0004803
文献
http://purl.org/net/cito/citesAsAuthority
Harumichi. Ishigame, et.al., Excessive Th1 responses due to the absence of TGF-β signaling cause autoimmune diabetes and dysregulated Treg cell homeostasis., Proceedings of the National Academy of Sciences of the United States of America, 2013, 110
http://rdf.ncbi.nlm.nih.gov/pubmed/23569233
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