期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 277, 期 37, 页码 34223-34228出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M201638200
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资金
- NHLBI NIH HHS [K08 HL 04287] Funding Source: Medline
Nitrosative stress produced by cytokines predisposes to apoptotic cell death. However, the molecular mechanism by which this occurs is not well understood. We have shown previously that nitric oxide (NO) regulates the activity of the anti-apoptotic transcription factor NF-kappaB. Here we demonstrate that the inhibition of NF-kappaB by NO sensitizes A549 and Jurkat T cells to tumor necrosis factor-alpha (TNFalpha)-induced apoptosis. The molecular basis of NF-kappaB inhibition is different in the two cell types. In A549 cells, NO functions at the nuclear level to inhibit NF-kappaB by S-nitrosylation. In Jurkat cells, NO inhibits the NF-kappaB activating pathway in the cytoplasm at a step proximal to the degradation of IkappaBalpha. The inhibition of NF-kappaB is reflected in the level of intracellular S-nitrosothiols, which are constitutively metabolized. These data suggest that NO can influence cell death by modulating NF-kappaB activity with the sites of inhibition being cell type-specific. The data also show that NO bioactivity regulates tumor necrosis factor-a signaling.
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