期刊
NATURE IMMUNOLOGY
卷 1, 期 4, 页码 342-347出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/79801
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资金
- NIAID NIH HHS [1PO1 AI44220-02] Funding Source: Medline
- NIGMS NIH HHS [GM29379, GM59919] Funding Source: Medline
We have generated, by ethylmethane sulfonate mutagenesis, loss-of-function mutants in the Drosophila homolog of the mammalian I-kappa B kinase (IKK) complex component IKK gamma (also called NEMO). Our data show that Drosophila IKK gamma is required for the Relish-dependent immune induction of the genes encoding antibacterial peptides and for resistance to infections by Escherichia coli. However, it is not required for the Toll-Dip-dependent antifungal host: defense,The results indicate distinct control mechanisms of the Rel-like transactivators DIF and Relish in the Drosophila innate immune response and show that Drosophila Toll does not signal through a IKK gamma-dependent signaling complex. Thus, in contrast to the vertebrate inflammatory response, IKK gamma is required for the activation of only one immune signaling pathway in Drosophila.
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