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Comparison of mouse and human NASP genes and expression in human transformed and tumor cell lines

We previously cloned and sequenced cDNAs encoding mouse NASP ( mNASP), a cell cycle regulated histone H1 binding protein. Here we report the genomic sequence and organization for mNASP along with its 5′ regulatory region and compare these with human NASP ( hNASP). The mNASP gene contains 16 exons in...

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Bibliographic Details
Published in:Gene 2001-08, Vol.274 (1), p.67-75
Main Authors: Richardson, Richard T., Bencic, David C., O'Rand, Michael G.
Format: Article
Language:English
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Summary:We previously cloned and sequenced cDNAs encoding mouse NASP ( mNASP), a cell cycle regulated histone H1 binding protein. Here we report the genomic sequence and organization for mNASP along with its 5′ regulatory region and compare these with human NASP ( hNASP). The mNASP gene contains 16 exons interrupted by 15 introns. The sequence encoding testis mNASP uses all 16 exons while the somatic form uses 13 exons by differential splicing. All the exons conform to the AG/GT splicing rule. Putative TATA box-containing transcription initiation sites are present for somatic NASP in human and mouse and for testis hNASP. Comparison of the promoter regions of mNASP and hNASP approximately 1 kb upstream of the transcription start sites for the two splice variants revealed a number of possible transcription factor binding sites relevant to specific patterns of NASP tissue expression. The presence of single bands on Southern blots of mouse genomic DNA suggests that mNASP is a single copy gene although pseudogenes exist in both the mouse and human genomes. Chromosome fluorescence by in situ hybridization revealed that mNASP is present on chromosome 4, in an area that corresponds to band 4D1, a region syntenic to the locus of hNASP on chromosome 1. Additionally, we report that human somatic and testis NASP mRNAs are expressed at varying levels in all the transformed cell lines and human tumors tested, further supporting NASP's role in the cell cycle of dividing cells.
ISSN:0378-1119
1879-0038
DOI:10.1016/S0378-1119(01)00605-9