PubMed · 12374949
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James L Sherley. 2002-10-10. Metastasis: objections to the same-gene model.. https://doi.org/10.1038/419560a
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Analysis of Saccharomyces cerevisiae cell transcriptome revealed that iron deprivation/supplementation affects genes other than those of the iron regulon (controlled by Aft proteins). Several genes regulated by zinc (induced by zinc deprivation) were induced by iron. Cells lacking the yeast frataxin homologue Yfh1 accumulate large amounts of iron in their mitochondria. We have shown that the zinc metabolism of these cells is also impaired: zinc uptake and zinc accumulation were both much lower in Delta yfh1 cells than in wild-type cells. Excess zinc in the growth medium also influenced the phenotypes of Delta yfh1 cells. It prevented the accumulation of iron in the mitochondria of Delta yfh1 cells and increased the growth rate of these cells and their resistance to oxidative stress. However, zinc did not restore the deficiency of Fe-S and haem proteins of Delta yfh1 cells. Zinc inhibited mitochondrial respiration and protected Yah1p, the mitochondrial ferredoxin. These results suggest that zinc nutrition may be important in the aetiology of Friedreich's ataxia.
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Human natural killer (NK) cell lines (YT and NK-92) and freshly isolated human NK cells were used to determine signal pathway (s) and their cytolysis-related molecules involved in IFNalpha-stimulated natural cytotoxicity. NK cells displayed apparently augmented cytotoxicity against target tumor cells (K562) and up-regulated gene expression of cytolytic effectors Fas-L and perforin in response to IFNalpha stimulation. Meanwhile, the tyrosine phosphorylation of STAT1 of NK cells was quickly induced, but other pathways including STAT3, STAT6, ERK1/2, p38 MAPK, JNK/SAPK, PI-3K, NF-kappaB were not or only weakly activated. Transient expression of dominant-negative form of STAT1 (DN STAT1) markedly inhibited STAT1 activation and then alleviated cytolysis activity of IFNalpha-treated YT cells, which was correlated to a markedly down-regulated expression of IRF-1, a key transcription factor necessary for cytotoxicity of IFNalpha/beta-activated NK cells. The results indicate that STAT1 activation play a crucial role in IFNalpha signaling for cytolysis function of NK cells.