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- W4313333656 abstract "Abstract Unmethylated CpG dinucleotides in particular base contexts in oligonucleotides (CpG DNA) rescue WEHI-231 cells from anti-IgM-induced cell cycle arrest and apoptosis. Anti-IgM rapidly elevated the levels of NFκB p50/c-Rel heterodimers followed by a decline of p50/c-Rel heterodimers by 3 h and a concomitant increase of p50/p50 homodimers. In contrast, CpG DNA induced and maintained the levels of p50/c-Rel heterodimers in the presence or absence of anti-IgM, while control non-CpG DNA failed to induce NFκB activation. Anti-IgM induced IκBα degradation followed by increased IκBα protein levels. The levels of IκBβ were increased after anti-IgM treatment. In contrast, CpG DNA, but not non-CpG DNA, induced sustained IκBα and IκBβ degradation in the presence or absence of anti-IgM. Inhibition of IκB degradation blocked CpG DNA-induced NFκB activation and expression of c-myc. Prevention of NFκB activation by inhibiting IκB degradation also suppressed the ability of CpG DNA to rescue WEHI-231 cells from anti-IgM-induced apoptosis. These results indicate that CpG DNA-mediated sustained activation of NFκB depends on the degradation of IκBα and IκBβ and is required for the CpG DNA-mediated anti-apoptosis gene expression and the protection against anti-IgM-induced apoptosis of WEHI-231 cells." @default.
- W4313333656 created "2023-01-06" @default.
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- W4313333656 date "1998-02-01" @default.
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- W4313333656 title "CpG DNA Rescue from Anti-IgM-Induced WEHI-231 B Lymphoma Apoptosis via Modulation of IκBα and IκBβ and Sustained Activation of Nuclear Factor-κB/c-Rel" @default.
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- W4313333656 doi "https://doi.org/10.4049/jimmunol.160.3.1240" @default.
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