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Titolo:
Genetic linkage analysis of X-ray hypersensitivity in the LEC mutant rat
Autore:
Agui, T; Miyamoto, T; Jung, CG; Tsumagari, T; Masuda, K; Manabe, T;
Indirizzi:
Nagoya City Univ, Sch Med, Ctr Expt Anim Sci, Nagoya, Aichi 4688601, JapanNagoya City Univ Nagoya Aichi Japan 4688601 Nagoya, Aichi 4688601, Japan KAC Co Ltd, Kyoto 6048423, Japan KAC Co Ltd Kyoto Japan 6048423KAC Co Ltd, Kyoto 6048423, Japan Nagoya City Univ, Sch Med, Dept Surg 1, Nagoya, Aichi 4688601, Japan Nagoya City Univ Nagoya Aichi Japan 4688601 Nagoya, Aichi 4688601, Japan
Titolo Testata:
MAMMALIAN GENOME
fascicolo: 10, volume: 11, anno: 2000,
pagine: 862 - 865
SICI:
0938-8990(200010)11:10<862:GLAOXH>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT PROTEIN-KINASE; HELPER IMMUNODEFICIENCY THID; MESSENGER-RNA EXPRESSION; STRAND BREAK REPAIR; EVANS CINNAMON RATS; WILSON-DISEASE GENE; V(D)J RECOMBINATION; HOMOLOGOUS RECOMBINATION; HEREDITARY HEPATITIS; IONIZING-RADIATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Agui, T Nagoya City Univ, Sch Med, Ctr Expt Anim Sci, Nagoya, Aichi 4688601, Japan Nagoya City Univ Nagoya Aichi Japan 4688601 Aichi 4688601, Japan
Citazione:
T. Agui et al., "Genetic linkage analysis of X-ray hypersensitivity in the LEC mutant rat", MAMM GENOME, 11(10), 2000, pp. 862-865

Abstract

The LEC rat has been reported to exhibit X-ray hyper sensitivity and deficiency in DNA double-strand break (DSB) repair. The present study was performed to map the locus responsible for this phenotype, the xhs (X-ray hypersensitivity), as the first step in identifying the responsible gene. Analysisof the progeny of (BN x LEC)F-1 x LEC backcrosses indicated that the X-rayhypersensitive phenotype was controlled by multiple genetic loci in contrast to the results reported previously. Quantitative trait loci (QTL) linkage analysis revealed two responsible loci located on Chromosomes (Chr) 4 and1. QTL on Chr 4 exhibited very strong linkage to the X-ray hypersensitive phenotype, while QTL on Chr 1 showed weak linkage. The Rad52 locus, mutation of which results in hypersensitivity to ionizing radiation and impairmentof DNA DSB repair in yeast, was reported to be located on the synteneic regions of mouse Chr 6 and human Chr 12. However, mapping of the rat Rad52 locus indicated that it was located 23 cM distal to the QTL on Chr 4. Furthermore, none of the radiosensitivity-related loci mapped previously in the rat chromosome were identical to the QTL on Chrs 4 and 1 in the LEC rat. Thus, it seems that X-ray hypersensitivity in the LEC rat is caused by mutation(s) in as-yet-undefined genes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 01:23:27