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| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C1171312 | lld:lifeskim |
| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C1623209 | lld:lifeskim |
| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C1419808 | lld:lifeskim |
| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C1423836 | lld:lifeskim |
| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C2755105 | lld:lifeskim |
| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C1334043 | lld:lifeskim |
| pubmed-article:16790473 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:16790473 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:16790473 | pubmed:dateCreated | 2006-7-12 | lld:pubmed |
| pubmed-article:16790473 | pubmed:abstractText | Mutations in SALL4, the human homolog of the Drosophila homeotic gene spalt (sal), cause the autosomal dominant disorder known as Okihiro syndrome. In this study, we show that a targeted null mutation in the mouse Sall4 gene leads to lethality during peri-implantation. Growth of the inner cell mass from the knockout blastocysts was reduced, and Sall4-null embryonic stem (ES) cells proliferated poorly with no aberrant differentiation. Furthermore, we demonstrated that anorectal and heart anomalies in Okihiro syndrome are caused by Sall4 haploinsufficiency and that Sall4/Sall1 heterozygotes exhibited an increased incidence of anorectal and heart anomalies, exencephaly and kidney agenesis. Sall4 and Sall1 formed heterodimers, and a truncated Sall1 caused mislocalization of Sall4 in the heterochromatin; thus, some symptoms of Townes-Brocks syndrome caused by SALL1 truncations could result from SALL4 inhibition. | lld:pubmed |
| pubmed-article:16790473 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16790473 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16790473 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16790473 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16790473 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16790473 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:16790473 | pubmed:issn | 0950-1991 | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:AsashimaMakot... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:YoshidaNobuak... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:KodamaTatsuhi... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:AburataniHiro... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:SatoAkiraA | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:MatsumotoYuko... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:KobayashiChiy... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:Nishinakamura... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:TakasatoMinor... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:Sakaki-Yumoto... | lld:pubmed |
| pubmed-article:16790473 | pubmed:author | pubmed-author:FujimuraSayok... | lld:pubmed |
| pubmed-article:16790473 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16790473 | pubmed:volume | 133 | lld:pubmed |
| pubmed-article:16790473 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16790473 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16790473 | pubmed:pagination | 3005-13 | lld:pubmed |
| pubmed-article:16790473 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:16790473 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16790473 | pubmed:articleTitle | The murine homolog of SALL4, a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development. | lld:pubmed |
| pubmed-article:16790473 | pubmed:affiliation | Division of Integrative Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan. | lld:pubmed |
| pubmed-article:16790473 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16790473 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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