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Titolo:
Variations in Prkdc encoding the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) and susceptibility to radiation-induced apoptosis and lymphomagenesis
Autore:
Mori, N; Matsumoto, Y; Okumoto, M; Suzuki, N; Yamate, J;
Indirizzi:
Adv Sci & Technol Res Inst, Dept Appl Biosci, Osaka 5998570, Japan Adv Sci& Technol Res Inst Osaka Japan 5998570 sci, Osaka 5998570, Japan Univ Osaka Prefecture, Coll Agr, Dept Vet Pathol, Osaka 5998570, Japan Univ Osaka Prefecture Osaka Japan 5998570 t Pathol, Osaka 5998570, Japan Univ Tokyo, Grad Sch Med, Dept Radiat Oncol, Bunkyo Ku, Tokyo 1130033, Japan Univ Tokyo Tokyo Japan 1130033 at Oncol, Bunkyo Ku, Tokyo 1130033, Japan
Titolo Testata:
ONCOGENE
fascicolo: 28, volume: 20, anno: 2001,
pagine: 3609 - 3619
SICI:
0950-9232(20010621)20:28<3609:VIPETC>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
SEVERE COMBINED IMMUNODEFICIENCY; COMBINED IMMUNE-DEFICIENCY; RECOMBINANT CONGENIC STRAINS; V(D)J RECOMBINATION; X-IRRADIATION; NONSENSE MUTATION; SCID MUTATION; BREAK REPAIR; MICE; THYMOCYTES;
Keywords:
apoptosis susceptibility; susceptibility to radiation lymphomagenesis; genetic variation in DNA-PKcs; DNA double-strand breaks repair;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Mori, N Adv Sci & Technol Res Inst, Dept Appl Biosci, Osaka 5998570, JapanAdv Sci & Technol Res Inst Osaka Japan 5998570 ka 5998570, Japan
Citazione:
N. Mori et al., "Variations in Prkdc encoding the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) and susceptibility to radiation-induced apoptosis and lymphomagenesis", ONCOGENE, 20(28), 2001, pp. 3609-3619

Abstract

DNA double-strand breaks (DSBs) induced by ionizing radiation enforce cells to die, if unrepaired; while if misrepaired, DSBs may cause malignant transformation. The DSB repair system predominant in mammals requires DNA-dependent protein kinase (DNA-PK), Previously, we identified the apoptosis susceptibility gene Radiation-induced apoptosis 1 (Rapop1) on mouse chromosome 16, The STS/A (STS) allele at Rapop1 leads to decreased sensitivity to apoptosis in the BALB/cHeA (BALB/c) background. In the present study, we established Rapop1 congenic strains C,S-RI and C.S-R1L, which contain the STS genome in a 0.45 cM interval critical for Rapop1 in common in the BALB/c background. Within the segment critical for Rapop1, Prkdc encoding the catalyticsubunit of DNA-PK (DNA-PKcs) was assigned. Two variations T6,418C and G11,530A, which induce amino acid substitutions C2,140R downstream from the putative leucine zipper motif and V3,844M near the kinase domain, respectively, were found between BALB/c and STS for Prkdc. The majority of inbred strains such as C57BL/6J carried the STS allele at Prkdc; a few strains including 129/SvJ and C.B17 carried the BALB/c allele. DNA-PK activity as well as DNA-PKcs expression was profoundly diminished in BALB/c and 129/SvJ mice as compared with C57BL/6 and C.S-R1 mice. In the crosses (C.S-R1 x BALB/c)F-1 x 129/SvJ and (C.S-R1 x BALB/c)F-1 x C.B17, enhanced apoptosis occurred in the absence of the wildtype allele at Prkdc. C.S-R1 and C.S-R1L were both less sensitive to radiation lymphomagenesis than BALB/ c, Our study providesstrong evidence for Prkdc as a candidate for Rapop1 and a susceptibility gene for radiation lymphomagenesis as well.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 01:08:19