Transcription of the RelB gene is regulated by NF-κB

Bren, Gary D.; Solan, Nancie J.; Miyoshi, Hideyuki; Pennington, Kevin N.; Pobst, Lori J.; Payá, Carlos V.

doi:10.1038/sj.onc.1204868

Cited by 194 publications

(182 citation statements)

References 43 publications

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“…TNF treatment for 3 h also resulted in an increase in p100 and RelB levels. This was in agreement with previous studies that described the degradation and resynthesis of IB␣ and the induction of p100 and RelB by the classical NF-B signaling pathway following TNF treatment (19). In contrast, a reduction of p100 was observed 3 h after the treatment with agonistic LT␤R mAb (compare lanes 1 and 6 -9) with a corresponding increase in nuclear p52 (Fig.…”

Section: Resultssupporting

confidence: 93%

Recruitment of RelB to the Csf2 Promoter Enhances RelA-mediated Transcription of Granulocyte-Macrophage Colony-stimulating Factor

Sasaki

Ghosh

Longo

2011

Journal of Biological Chemistry

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Tumor necrosis factor (TNF) induces expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) but lymphotoxin ␤ (LT␤) does not. Here we report that priming of cells with agonistic LT␤ receptor antibody synergistically enhanced TNF-induced GM-CSF expression. The LT␤ priming process was not due to an increase in TNF-mediated nuclear translocation of p65, p65 DNA binding, or NF-B transactivational activity. The synergistic effect of LT␤ priming was not observed with other TNF-responsive genes such as Ccl2 or RelB, which suggested that this effect was not a general increase in TNF signaling. Furthermore, RelB and p65 were both independently recruited to the GM-CSF promoter when cells were primed with LT␤ followed by TNF treatment. As a consequence, an increase in both chromatin accessibility and the recruitment of RNA polymerase II were observed to the GM-CSF promoter. Taken together, these findings suggested that LT␤ signaling amplified TNF-mediated GM-CSF expression by facilitating chromatin access and the co-recruitment of RNA polymerase II to increase gene transcription. Moreover, the novel priming process described here underscores the complexity of the interactions between the classical and alternative NF-B signaling pathways.

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Section: Resultssupporting

confidence: 93%

Recruitment of RelB to the Csf2 Promoter Enhances RelA-mediated Transcription of Granulocyte-Macrophage Colony-stimulating Factor

Sasaki

Ghosh

Longo

2011

Journal of Biological Chemistry

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“…Early studies showed that the promoter regions of relb and nfκb2 genes contain κB-binding sites and transcriptional regulation of these two genes is dependent on RelA [105,106]. LTβR signaling was shown to activate RelA:p50 followed by RelB:p52 via two distinct pathways [107].…”

Section: Rela:p50 Control Of Non-canonical Signalingmentioning

confidence: 99%

A single NFκB system for both canonical and non-canonical signaling

et al. 2010

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Two distinct nuclear factor κB (NFκB) signaling pathways have been described; the canonical pathway that mediates inflammatory responses, and the non-canonical pathway that is involved in immune cell differentiation and maturation and secondary lymphoid organogenesis. The former is dependent on the IκB kinase adaptor molecule NEMO, the latter is independent of it. Here, we review the molecular mechanisms of regulation in each signaling axis and attempt to relate the apparent regulatory logic to the physiological function. Further, we review the recent evidence for extensive cross-regulation between these two signaling axes and summarize them in a wiring diagram. These observations suggest that NEMO-dependent and -independent signaling should be viewed within the context of a single NFκB signaling system, which mediates signaling from both inflammatory and organogenic stimuli in an integrated manner. As in other regulatory biological systems, a systems approach including mathematical models that include quantitative and kinetic information will be necessary to characterize the network properties that mediate physiological function, and that may break down to cause or contribute to pathology.

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“…Thus, RelB binding to the MnSOD promoter may allow for more accessibility for binding of other transcription factors including Sp1 (Xu et al, 2002) and coactivators (nucleophosmin) (Dhar et al, 2004). RelB itself could activate its own gene (Bren et al, 2001) and additional transcription factors to activate the MnSOD gene in response to radiation. Consistent with the induction of MnSOD, a time-dependent increase in MnSOD protein was observed paralleling the MnSOD mRNA levels Figure 1 Increased nuclear protein levels of RelB correlate with intrinsic radiation resistance.…”

Section: Relb Enhances Radiation Resistance S Josson Et Almentioning

confidence: 99%

RelB regulates manganese superoxide dismutase gene and resistance to ionizing radiation of prostate cancer cells

Josson

Fang

et al. 2005

Oncogene

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The relationship between NF-jB and resistance to radiation treatment in many tumor cell types has been generally well recognized. However, which members of the NF-jB family contribute to radiation resistance is unclear.In the present study, we demonstrate that RelB plays an important radioprotective role in aggressive prostate cancer cells, in part by the induction of antioxidant and antiapoptotic manganese superoxide dismutase (MnSOD) gene. RelB is both constitutively present and is inducible by radiation in aggressive prostate cancer cells. Using ectopically expressed dominant negative inhibitor, p100 mutant, and the siRNA approach, we demonstrate that selective inhibition of RelB significantly decreases the levels of MnSOD resulting in a significant increase in the sensitivity of prostate cancer cells to radiation treatment. These results demonstrate that RelB plays an important role in redox regulation of the cell and protects aggressive prostate cancer cells against radiation-induced cell death. Thus, inhibition of RelB could be a novel mechanism to radiosensitize prostate cancer.

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Transcription of the RelB gene is regulated by NF-κB

Cited by 194 publications

References 43 publications

Recruitment of RelB to the Csf2 Promoter Enhances RelA-mediated Transcription of Granulocyte-Macrophage Colony-stimulating Factor

Recruitment of RelB to the Csf2 Promoter Enhances RelA-mediated Transcription of Granulocyte-Macrophage Colony-stimulating Factor

A single NFκB system for both canonical and non-canonical signaling

RelB regulates manganese superoxide dismutase gene and resistance to ionizing radiation of prostate cancer cells

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