Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease
Transforming growth factor-β1 (TGF-β1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-β1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disru...
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Veröffentlicht in: | Nature (London) 1992-10, Vol.359 (6397), p.693-699 |
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creator | Shull, Marcia M. Ormsby, Ilona Kier, Ann B. Pawlowski, Sharon Diebold, Ronald J. Yin, Moying Allen, Ruth Sidman, Charles Proetzel, Gabriele Calvin, Dawn Annunziata, Nikki Doetschman, Thomas |
description | Transforming growth factor-β1 (TGF-β1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-β1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-β1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-β1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions. |
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Disruption of the TGF-β1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-β1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-β1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/359693a0</identifier><identifier>PMID: 1436033</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Biochemistry ; Biological and medical sciences ; Experimental and animal immunopathology. Animal models ; Humanities and Social Sciences ; Immunity (Disease) ; Immunopathology ; Medical research ; Medical sciences ; multidisciplinary ; Rodents ; Science ; Science (multidisciplinary) ; Stem cells</subject><ispartof>Nature (London), 1992-10, Vol.359 (6397), p.693-699</ispartof><rights>Springer Nature Limited 1992</rights><rights>1993 INIST-CNRS</rights><rights>Copyright Macmillan Journals Ltd. Oct 22, 1992</rights><rights>1992 Nature Publishing Group 1992</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3850-e5ceced0aae0009014b963da0b5ac0f7146aecd081e900089684dccfc0b434903</citedby><cites>FETCH-LOGICAL-c3850-e5ceced0aae0009014b963da0b5ac0f7146aecd081e900089684dccfc0b434903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/359693a0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/359693a0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4374739$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Shull, Marcia M.</creatorcontrib><creatorcontrib>Ormsby, Ilona</creatorcontrib><creatorcontrib>Kier, Ann B.</creatorcontrib><creatorcontrib>Pawlowski, Sharon</creatorcontrib><creatorcontrib>Diebold, Ronald J.</creatorcontrib><creatorcontrib>Yin, Moying</creatorcontrib><creatorcontrib>Allen, Ruth</creatorcontrib><creatorcontrib>Sidman, Charles</creatorcontrib><creatorcontrib>Proetzel, Gabriele</creatorcontrib><creatorcontrib>Calvin, Dawn</creatorcontrib><creatorcontrib>Annunziata, Nikki</creatorcontrib><creatorcontrib>Doetschman, Thomas</creatorcontrib><title>Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease</title><title>Nature (London)</title><addtitle>Nature</addtitle><description>Transforming growth factor-β1 (TGF-β1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-β1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-β1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-β1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.</description><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Experimental and animal immunopathology. 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Disruption of the TGF-β1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-β1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-β1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>1436033</pmid><doi>10.1038/359693a0</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biochemistry Biological and medical sciences Experimental and animal immunopathology. Animal models Humanities and Social Sciences Immunity (Disease) Immunopathology Medical research Medical sciences multidisciplinary Rodents Science Science (multidisciplinary) Stem cells |
title | Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease |
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