pubmed-article:16943438 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16943438 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
pubmed-article:16943438 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:16943438 | lifeskim:mentions | umls-concept:C0020507 | lld:lifeskim |
pubmed-article:16943438 | lifeskim:mentions | umls-concept:C0597298 | lld:lifeskim |
pubmed-article:16943438 | lifeskim:mentions | umls-concept:C0205480 | lld:lifeskim |
pubmed-article:16943438 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:16943438 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
pubmed-article:16943438 | pubmed:issue | 18 | lld:pubmed |
pubmed-article:16943438 | pubmed:dateCreated | 2006-8-31 | lld:pubmed |
pubmed-article:16943438 | pubmed:abstractText | Alternative splicing in the BRCA1 locus generates multiple protein products including BRCA1-Delta11, which is identical to the BRCA1 full-length isoform (BRCA1-FL) except for the absence of exon 11. Mutation analysis using gene targeting to create null mutations or disrupt BRCA-FL has provided much of our understanding of BRCA1 functions; however, targeted mutation of specific short forms of BRCA1 has not been reported. To understand the physiologic functions of BRCA1-Delta11, we used a knock-in approach that blocks alternative splicing between exons 10 and 12 to prevent the formation of this form of BRCA1. We showed that homozygous mutant mice (Brca1(FL/FL)) were born at a Mendelian ratio without obvious developmental defects. However, the majority of Brca1(FL/FL) female mice showed mammary gland abnormalities and uterine hyperplasia after one year of age with spontaneous tumor formation. Cultured Brca1(FL/FL) cells exhibited abnormal centrosome amplification and reduction of G(1) population that was accompanied by accumulation of cyclin E and cyclin A. Accumulation of cyclin E was also found in epithelial layers of dilated ducts and hyperproliferative lobular regions in the mammary glands of Brca1(FL/FL) mice. These observations provide evidence that BRCA1 splicing variants are involved in BRCA1 functions in modulating G(1)/S transition, centrosome duplication, and repressing tumor formation. | lld:pubmed |
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pubmed-article:16943438 | pubmed:language | eng | lld:pubmed |
pubmed-article:16943438 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16943438 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16943438 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:16943438 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16943438 | pubmed:month | Sep | lld:pubmed |
pubmed-article:16943438 | pubmed:issn | 0270-7306 | lld:pubmed |
pubmed-article:16943438 | pubmed:author | pubmed-author:LimSung-ChulS... | lld:pubmed |
pubmed-article:16943438 | pubmed:author | pubmed-author:DengChu-XiaCX | lld:pubmed |
pubmed-article:16943438 | pubmed:author | pubmed-author:LiCuilingC | lld:pubmed |
pubmed-article:16943438 | pubmed:author | pubmed-author:XuXiaolingX | lld:pubmed |
pubmed-article:16943438 | pubmed:author | pubmed-author:BachelierRich... | lld:pubmed |
pubmed-article:16943438 | pubmed:author | pubmed-author:DJUM YMY | lld:pubmed |
pubmed-article:16943438 | pubmed:author | pubmed-author:KimSang SooSS | lld:pubmed |
pubmed-article:16943438 | pubmed:author | pubmed-author:WangRui-HongR... | lld:pubmed |
pubmed-article:16943438 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16943438 | pubmed:volume | 26 | lld:pubmed |
pubmed-article:16943438 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16943438 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16943438 | pubmed:pagination | 6983-92 | lld:pubmed |
pubmed-article:16943438 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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