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R. Ippoliti P. Ginobbi E. Lendaro I. D'Agostino D. Ombres P. A. Benedetti M. Brunori G. Citro 《Cellular and molecular life sciences : CMLS》1998,54(8):866-875
The toxicity of two conjugates containing ribosome-inactivating proteins (RIPs, i.e. saporin and ricin-A chain x-linked to
transferrin) has been measured on a prostatic cancer line (PC3) naturally overexpressing the transferrin receptor, in the
presence of monensin and chloroquine. This paper investigates whether the increased toxicity of Tf-RIPs induced by monensin
and chloroquine may be due to alterations of the normal endocytotic pathway of the complexes mediated by the transferrin receptor.
Monensin, besides inducing alkalinization of normally acid intracellular compartments, causes an accumulation of the receptor-bound
Tf-RIP in a perinuclear region contiguous to the cisternae of the trans-Golgi network. Chloroquine, though increasing the
intracellular pH, seems not to modify the endocytotic pathway of these chimeric molecules. We believe that the enhanced toxicity
of the Tf-RIPs may be related to intracellular alkalinization (i.e. endosomal or lysosomal pH) rather than to the effects
on the recycling of transferrin receptor-bound toxins. We conclude that the efficacy of chimeric toxins may be modulated not
only by the carrier used for their engineering but also by addition of drugs able to influence the stability and activation
of the toxins inside the cell.
Received 22 December 1997; received after revision 30 March 1998; accepted 15 May 1998 相似文献
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Rioux JD Xavier RJ Taylor KD Silverberg MS Goyette P Huett A Green T Kuballa P Barmada MM Datta LW Shugart YY Griffiths AM Targan SR Ippoliti AF Bernard EJ Mei L Nicolae DL Regueiro M Schumm LP Steinhart AH Rotter JI Duerr RH Cho JH Daly MJ Brant SR 《Nature genetics》2007,39(5):596-604
We present a genome-wide association study of ileal Crohn disease and two independent replication studies that identify several new regions of association to Crohn disease. Specifically, in addition to the previously established CARD15 and IL23R associations, we identified strong and significantly replicated associations (combined P < 10(-10)) with an intergenic region on 10q21.1 and a coding variant in ATG16L1, the latter of which was also recently reported by another group. We also report strong associations with independent replication to variation in the genomic regions encoding PHOX2B, NCF4 and a predicted gene on 16q24.1 (FAM92B). Finally, we demonstrate that ATG16L1 is expressed in intestinal epithelial cell lines and that functional knockdown of this gene abrogates autophagy of Salmonella typhimurium. Together, these findings suggest that autophagy and host cell responses to intracellular microbes are involved in the pathogenesis of Crohn disease. 相似文献
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