| http://purl.uniprot.org/citations/22383537 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22383537 | http://www.w3.org/2000/01/rdf-schema#comment | "Smad7 is an inhibitory molecule induced by members of the transforming growth factor-β (TGF-β) family, including TGF-β, activin, nodal and bone morphogenetic proteins (BMPs). To elucidate the in vivo functions of Smad7, we generated conditional Smad7-knockout mice in which the Mad homology 2 (MH2) domain and the poly (A) signal sequence were flanked with loxP sites (floxed). The Smad7-floxed mice exhibited no obvious phenotype. Smad7 total-null mice on a C57BL/6 background died within a few days of birth, whereas mice with an ICR background developed to adulthood but were significantly smaller than wild-type mice. Unexpectedly, phospho-Smad2 and phospho-Smad3 were decreased in Smad7-deficient mouse embryonic fibroblast (MEF) cells, whereas phospho-Smad1/5/8 was similarly expressed in wild-type and Smad7-deficient MEF cells. Moreover, expression levels of TGF-β type I receptor (ALK5) were higher in Smad7-deficient MEF cells than in wild-type MEF cells. Plasminogen activator inhibitor-1 (PAI-1) and inhibitor of differentiation-1 (Id-1) mRNA were similarly expressed in wild-type and Smad7-deficient MEF cells. Some differences were observed in mitogen-activated protein kinase (MAPK)-signalling between wild-type and Smad7-deficient MEF cells. We demonstrated that Smad7 plays an important role in normal mouse growth and provide a useful tool for analysing Smad7 functions in vivo."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.org/dc/terms/identifier | "doi:10.1093/jb/mvs022"xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/author | "Tanaka K."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/author | "Takahashi S."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/author | "Imamura T."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/author | "Chiba T."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/author | "Miyazono K."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/author | "Takebe A."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/author | "Tojo M."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/name | "J Biochem"xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/pages | "621-631"xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/title | "Smad7-deficient mice show growth retardation with reduced viability."xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://purl.uniprot.org/core/volume | "151"xsd:string |
| http://purl.uniprot.org/citations/22383537 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22383537 |
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