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Titolo:
Modulations of glucocorticoid-induced apoptosis linked to the p53 deletionand to the apoptosis susceptibility gene Rapop1 (Radiation-induced apoptosis 1)
Autore:
Mori, N; Yamate, J; Stassen, APM; Oka, S; Okumoto, H; Tsubura, A; Akamatsu, T; Sakuma, S; Demant, P;
Indirizzi:
Univ Osaka Prefecture, Dept Appl Biosci, Res Inst Adv Sci & Technol, Sakai, Osaka 5998570, Japan Univ Osaka Prefecture Sakai Osaka Japan 5998570 kai, Osaka 5998570, Japan Univ Osaka Prefecture, Coll Agr, Dept Vet Pathol, Sakai, Osaka 5998531, Japan Univ Osaka Prefecture Sakai Osaka Japan 5998531 kai, Osaka 5998531, Japan Univ Osaka Prefecture, Coll Agr, Dept Vet Radiol, Sakai, Osaka 5998531, Japan Univ Osaka Prefecture Sakai Osaka Japan 5998531 kai, Osaka 5998531, Japan Kansai Med Univ, Dept Pathol, Moriguchi, Osaka 5700074, Japan Kansai Med Univ Moriguchi Osaka Japan 5700074 guchi, Osaka 5700074, Japan Netherlands Canc Inst, Div Mol Genet, NL-1066 CX Amsterdam, Netherlands Netherlands Canc Inst Amsterdam Netherlands NL-1066 CX rdam, Netherlands
Titolo Testata:
ONCOGENE
fascicolo: 29, volume: 18, anno: 1999,
pagine: 4282 - 4285
SICI:
0950-9232(19990722)18:29<4282:MOGALT>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECOMBINANT CONGENIC STRAINS; INDUCED THYMOCYTE APOPTOSIS; POSITIVE SELECTION; INHIBITION; RECEPTOR; IMMUNOSUPPRESSION; IDENTIFICATION; ACTIVATION; INVITRO; TUMORS;
Keywords:
p53; glucocorticoid-induced apoptosis; apoptosis susceptibility genes; genetic analysis; mouse;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Mori, N Univ Osaka Prefecture, Dept Appl Biosci, Res Inst Adv Sci & Technol, 1-2 Gakuen Cho, Sakai, Osaka 5998570, Japan Univ Osaka Prefecture 1-2 Gakuen Cho Sakai Osaka Japan 5998570 pan
Citazione:
N. Mori et al., "Modulations of glucocorticoid-induced apoptosis linked to the p53 deletionand to the apoptosis susceptibility gene Rapop1 (Radiation-induced apoptosis 1)", ONCOGENE, 18(29), 1999, pp. 4282-4285

Abstract

We have analysed the effects of p53 and of the apoptosis susceptibility gene Rapop1 (Radiation-induced apoptosis 1) located on chromosome 16 on glucocorticoid- and radiation-induced in vivo apoptosis of thymocytes. For thoseanalyses, we used Rapop1 semicongenic mice heterozygous for the STS and BALB/cHeA alleles in the chromosomal segment containing Rapop1 in the. BALB/cHeA background, mice bearing a p53 deficient allele in the BALB/cHeA background and the genetic crosses between these mice. The p53 wild type mice with a STS/A allele at the Rapop1 locus were less susceptible to both radiation- and glucocorticoid-induced apoptosis than those with homozygous BALB/cHeA alleles at this locus. Surprisingly, glucocorticoid-induced apoptosis wasenhanced in the p53 hemizygous mice and considerably increased in the p53 nullizygous mice. In contrast, a sizable reduction of radiation-induced apoptosis was seen in tbe p53 hemizygous mice, The low susceptibility to glucocortocoid-induced apoptosis linked to the STS allele of Rapop1 was less pronounced in the p53 hemizygous mice and a diminished effect of Rapop1 on radiation-induced apoptosis was seen in these mice. Although it remains to be established whether the genes modulating glucocortocoid-induced apoptosis are identical to g53 and Rapop1, our data suggest that p53 and Rapop1 may participate in glucocorticoid-induced apoptosis of thymocytes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 02:48:58