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Titolo:
Intron/exon organization and polymorphisms of the PLK3/PRK gene in human lung carcinoma cell lines
Autore:
Wiest, J; Clark, AM; Dai, W;
Indirizzi:
Univ Cincinnati, Coll Med, Dept Environm Hlth, Cincinnati, OH 45267 USA Univ Cincinnati Cincinnati OH USA 45267 nm Hlth, Cincinnati, OH 45267 USA
Titolo Testata:
GENES CHROMOSOMES & CANCER
fascicolo: 4, volume: 32, anno: 2001,
pagine: 384 - 389
SICI:
1045-2257(200112)32:4<384:IOAPOT>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALLELIC LOSS; NECK-CANCER; KINASE; 8P; HETEROZYGOSITY; PROGRESSION; EXPRESSION; HEAD; LOCI; PRK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Wiest, J Univ Cincinnati, Coll Med, Dept Environm Hlth, POB 670056, Cincinnati, OH 45267 USA Univ Cincinnati POB 670056 Cincinnati OH USA 45267 , OH 45267 USA
Citazione:
J. Wiest et al., "Intron/exon organization and polymorphisms of the PLK3/PRK gene in human lung carcinoma cell lines", GENE CHROM, 32(4), 2001, pp. 384-389

Abstract

PLK3/PRK, a conserved polo family protein serine/threonine kinase, plays asignificant role at the onset of mitosis and mitotic progression. Recently, PLK3/PRK has been shown to induce apoptosis when overexpressed in cell lines and is also implicated in cell proliferation and tumor development. Forty lung tumor cell lines were used for single-strand confirmation polymorphism (SSCP) analysis and DNA sequencing to examine the mutational status of PLK3/PRK. No missense or nonsense mutations were revealed in the lung carcinoma cell lines examined. However, three polymorphisms were identified as: a G to A at position 720, an A to G at 1053, and a G to C at 1275. Intron/exon boundaries were determined by amplification of genomic DNA with PLK3/PRK exon-specific primers. The amplification products with increased size relative to the cDNA were sequenced. Fifteen exons throughout the open readingframe were characterized. None of the introns were exceptionally large, typically ranging from 100-300 basepairs in length. These results suggest that although PLK3/PRK expression is downregulated in a majority of lung carcinoma samples, mutational inactivation of the coding sequence of the PLK3/PRK gene appears to be a rare event in lung cancer. (C) 2001 Wiley-Liss, Inc.

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Documento generato il 02/04/20 alle ore 00:28:31