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• W2127905124 abstract "Alternative splicing in the BRCA1 locus generates multiple protein products including BRCA1-Δ11, 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-Δ11, 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 (Brca1FL/FL) were born at a Mendelian ratio without obvious developmental defects. However, the majority of Brca1FL/FL female mice showed mammary gland abnormalities and uterine hyperplasia after one year of age with spontaneous tumor formation. Cultured Brca1FL/FL cells exhibited abnormal centrosome amplification and reduction of G1 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 Brca1FL/FL mice. These observations provide evidence that BRCA1 splicing variants are involved in BRCA1 functions in modulating G1/S transition, centrosome duplication, and repressing tumor formation." @default.
• W2127905124 created "2016-06-24" @default.
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• W2127905124 date "2006-09-01" @default.
• W2127905124 modified "2023-10-02" @default.
• W2127905124 title "Hyperplasia and Spontaneous Tumor Development in the Gynecologic System in Mice Lacking the BRCA1-Δ11 Isoform" @default.
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• W2127905124 doi "https://doi.org/10.1128/mcb.00796-06" @default.
• W2127905124 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1592852" @default.
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• W2127905124 hasPublicationYear "2006" @default.
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