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Differential basal synthesis of Hsp70/Hsc70 contributes to interindividual variation in Hsp70/Hsc70 inducibility 总被引:7,自引:0,他引:7
Boshoff T Lombard F Eiselen R Bornman JJ Bachelet M Polla BS Bornman L 《Cellular and molecular life sciences : CMLS》2000,57(8-9):1317-1325
The source of intraspecies variation in the expression of heat shock proteins (HSPs) remains unresolved but could shed light
on differential stress tolerance and disease susceptibility. This study investigated the influence of variable basal HSP synthesis
on differential inducibility of HSP synthesis. Basal and heat-induced synthesis of the major HSP families in peripheral blood
monocytes from healthy donors (n=42) were analysed using biometabolic labelling and densitometry. Basal Hsp70/Hsc70 synthesis
and percentage induction of Hsp70/Hsc70 synthesis were significantly correlated (r=−0.57, p<0.0001), and described most accurately
by an exponential decay equation (R=0.68, R2=0.46). This regression equation suggests that increasing levels of basal Hsp70/Hsc70 synthesis are accompanied byan exponential
decrease in the percentage induction of Hsp70/Hsc70 synthesis. The model fits data from European and non-European population
groups independently, although both coefficients in the regression equation were larger for non-Europeans. This implies population
group as an additional factor influencing differential HSP expression. The differential inducibility of Hsp70/Hsc70 due to
variable basal synthesis of Hsp70/Hsc70 and based upon population group may contribute to differential stress tolerance or
disease susceptibility.
Received 27 March 2000; received after revision 19 June 2000; accepted 20 June 2000 相似文献
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A. Lombard M. Buffa A. Manino A. Patetta 《Cellular and molecular life sciences : CMLS》1984,40(2):178-180
Summary The presence of small amounts of raffinose in the honeydew of 6 aphid species was demonstrated by means of TLC and GLC after invertase hydrolysis. The method allows the detection of this sugar even in the presence of a high percentage of melezitose.Work carried out under a C.N.R. grant. 相似文献
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Chang S Multani AS Cabrera NG Naylor ML Laud P Lombard D Pathak S Guarente L DePinho RA 《Nature genetics》2004,36(8):877-882
Mutational inactivation of the gene WRN causes Werner syndrome, an autosomal recessive disease characterized by premature aging, elevated genomic instability and increased cancer incidence. The capacity of enforced telomerase expression to rescue premature senescence of cultured cells from individuals with Werner syndrome and the lack of a disease phenotype in Wrn-deficient mice with long telomeres implicate telomere attrition in the pathogenesis of Werner syndrome. Here, we show that the varied and complex cellular phenotypes of Werner syndrome are precipitated by exhaustion of telomere reserves in mice. In late-generation mice null with respect to both Wrn and Terc (encoding the telomerase RNA component), telomere dysfunction elicits a classical Werner-like premature aging syndrome typified by premature death, hair graying, alopecia, osteoporosis, type II diabetes and cataracts. This mouse model also showed accelerated replicative senescence and accumulation of DNA-damage foci in cultured cells, as well as increased chromosomal instability and cancer, particularly nonepithelial malignancies typical of Werner syndrome. These genetic data indicate that the delayed manifestation of the complex pleiotropic of Wrn deficiency relates to telomere shortening. 相似文献
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