NF-κB Signaling

Dixit, Vishva M.; Mak, Tak W.

doi:10.1016/s0092-8674(02)01166-2

Cited by 193 publications

(58 citation statements)

References 14 publications

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“…genes encoding cytokines, chemokines, adhesion molecules, and antiapoptotic proteins (33). For a long time, NF B was considered to act exclusively as a mediator of cell survival, antagonizing cell death by up-regulation of antiapoptotic proteins.…”

Section: Differentially Influences the Expression Of Either Pro-or Anmentioning

confidence: 99%

NFκB-dependent Down-regulation of Tumor Necrosis Factor Receptor-associated Proteins Contributes to Interleukin-1-mediated Enhancement of Ultraviolet B-induced Apoptosis

Pöppelmann

Klimmek

Stróżyk

et al. 2005

Journal of Biological Chemistry

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Activation of the transcription factor nuclear factor-B (NF B) by inflammatory cytokines like tumor necrosis (TNF) factor and interleukin-1 (IL-1) is generally associated with the induction of antiapoptotic pathways. Therefore, NF B inhibits both intrinsically and extrinsically induced apoptosis and thus is regarded to act universally in an antiapoptotic fashion. Accordingly, activation of NF B by IL-1 was shown to result in reduction of death ligand-induced apoptosis via up-regulation of antiapoptotic inhibitor of apoptosis proteins (IAPs). In contrast, apoptosis induced by ultraviolet-B radiation (UVB) was shown to be enhanced in an NF B-dependent manner, indicating that NF B can also act in a proapoptotic fashion. This study investigates the molecular mechanisms underlying IL-1-mediated enhancement of UVB-induced apoptosis. We show that NF B activation in costimulation with UVB treatment results in repression of antiapoptotic genes and consequently in down-regulation of the respective proteins, like c-IAP, FLICE-inhibitory protein (FLIP), and some members of the TNF receptor-associated (TRAF)2 protein family. In parallel, TNF␣ is released, leading to activation of signaling pathways mediated by TNF receptor-1 (TNF-R1). Although TNF is well known to induce both proapoptotic and antiapoptotic effects, the down-regulated levels of TRAF-1, -2, and -6 proteins by IL-1 plus UVB action leads to a shift toward promotion of the proapoptotic pathway. In concert with the down-regulation of IAPs and FLIP, TNF-R1 activation as an additional proapoptotic stimulus now results in significant enhancement of UVB-induced apoptosis. Taken together, elucidation of the molecular mechanisms underlying IL-1-mediated enhancement of UVB-induced apoptosis revealed that NF B does not exclusively act in an antiapoptotic fashion but may also mediate proapoptotic effects.

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Section: Differentially Influences the Expression Of Either Pro-or Anmentioning

confidence: 99%

NFκB-dependent Down-regulation of Tumor Necrosis Factor Receptor-associated Proteins Contributes to Interleukin-1-mediated Enhancement of Ultraviolet B-induced Apoptosis

Pöppelmann

Klimmek

Stróżyk

et al. 2005

Journal of Biological Chemistry

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“…NF-kB can be activated by a variety of stimuli, including interleukin-1 (IL-1) and TNF-a, and among its multiple effects, it also induces antiapoptotic proteins (Dixit and Mak, 2002). Therefore, NF-kB was generally considered to act predominantly as a mediator of cell survival.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of NF-κB on apoptosis induced by DNA-damaging agents: the type of DNA damage determines the final outcome

et al. 2006

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“…A major challenge in the NF-B field is to understand how distinct upstream stimuli activate IKK in a signal-specific manner (5). Recently, the adapter and scaffold proteins Bcl10 and Malt1 were identified as specific regulators of T cell receptor-and B cell receptor-mediated NF-B activation (6).…”

mentioning

confidence: 99%

Bcl10 and Malt1 control lysophosphatidic acid-induced NF-κB activation and cytokine production

Klemm

Zimmermann

Peschel

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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NF-κB Signaling

Cited by 193 publications

References 14 publications

NFκB-dependent Down-regulation of Tumor Necrosis Factor Receptor-associated Proteins Contributes to Interleukin-1-mediated Enhancement of Ultraviolet B-induced Apoptosis

NFκB-dependent Down-regulation of Tumor Necrosis Factor Receptor-associated Proteins Contributes to Interleukin-1-mediated Enhancement of Ultraviolet B-induced Apoptosis

Differential effects of NF-κB on apoptosis induced by DNA-damaging agents: the type of DNA damage determines the final outcome

Bcl10 and Malt1 control lysophosphatidic acid-induced NF-κB activation and cytokine production

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