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- W859618145 abstract "Research Article1 September 1990free access Molecular cloning, primary structure and expression of the human X linked A1S9 gene cDNA which complements the ts A1S9 mouse L cell defect in DNA replication. E. Zacksenhaus E. Zacksenhaus Department of Microbiology, Faculty of Medicine, University of Toronto, Ontario, Canada. Search for more papers by this author R. Sheinin R. Sheinin Department of Microbiology, Faculty of Medicine, University of Toronto, Ontario, Canada. Search for more papers by this author E. Zacksenhaus E. Zacksenhaus Department of Microbiology, Faculty of Medicine, University of Toronto, Ontario, Canada. Search for more papers by this author R. Sheinin R. Sheinin Department of Microbiology, Faculty of Medicine, University of Toronto, Ontario, Canada. Search for more papers by this author Author Information E. Zacksenhaus1 and R. Sheinin1 1Department of Microbiology, Faculty of Medicine, University of Toronto, Ontario, Canada. The EMBO Journal (1990)9:2923-2929https://doi.org/10.1002/j.1460-2075.1990.tb07483.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info The temperature-sensitive ts A1S9 mutation of mouse L cells was previously shown to affect nuclear DNA replication and to be complemented by active and inactive human X chromosomes in human-ts A1S9 somatic cell hybrids. We report the isolation of cDNA clones which correct the ts A1S9 lesion, using as a probe a genomic fragment derived from the human A1S9 locus. The nucleotide sequence of the A1S9 cDNA encompasses a single open reading frame of 2409 bp which could encode a heretofore unreported protein of 90 393 daltons. Southern blot hybridization of the A1S9 cDNA probe with DNA from various species revealed homologous sequences in vertebrates but not in yeast. Northern blot analysis of serum-starved, synchronized cells demonstrated that the A1S9 gene was expressed at a relatively low level in quiescent cells and at a higher and constant level throughout the cell cycle. Human cell lines harbouring increasing numbers of inactive X chromosomes (47, XXX, 49, XXXXX) were found to express the A1S9 gene at the same level as control cells (45, X), suggesting that the gene does not escape X chromosome inactivation. Previous ArticleNext Article Volume 9Issue 91 September 1990In this issue RelatedDetailsLoading ..." @default.
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- W859618145 title "Molecular cloning, primary structure and expression of the human X linked A1S9 gene cDNA which complements the ts A1S9 mouse L cell defect in DNA replication." @default.
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- W859618145 doi "https://doi.org/10.1002/j.1460-2075.1990.tb07483.x" @default.
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