I kappa B epsilon, a novel member of the Ikappa B family, controls RelA and cRel NF-kappa B activity

Whiteside, Simon T.; Epinat, Jean‐Charles; Rice, Nancy R.; Israël, Alain

doi:10.1093/emboj/16.6.1413

Cited by 367 publications

(241 citation statements)

References 61 publications

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“…These include three inhibitors of NF-κB (IκBs), namely IκBα, -β and -ε (Li and Nabel, 1997;Whiteside et al, 1997;Zabel and Baeuerle, 1990), and two NF-κB precursor proteins, namely nfkb1 p105 and nfkb2 p100. Common to all five NF-κB inhibitors is the ankyrin repeat domain (ARD), which masks NF-κB DNA binding and nuclear translocation sequences (Huxford et al, 1998).…”

Section: The Nf-κb Signaling Systemmentioning

confidence: 99%

Crosstalk via the NF-κB signaling system

Basak¹,

Hoffmann²

2008

Cytokine & Growth Factor Reviews

153

117

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The NF-κB family of transcription factors consists of fifteen possible dimers whose activity is controlled by a family of inhibitor proteins, known as IκBs. A variety of cellular stimuli, many of them transduced by members of the TNFR superfamily, induce degradation of IκBs to activate an overlapping subset of NF-κB dimers. However, generation and stimulus-responsive activation of NF-κB dimers are intimately linked via various cross-regulatory mechanisms that allow crosstalk between different signaling pathways through the NF-κB signaling system. In this review, we summarize these mechanisms and discuss physiological and pathological consequences of crosstalk between apparently distinct inflammatory and developmental signals. We argue that a systems approach will be valuable for understanding questions of specificity and emergent properties of highly networked cellular signaling systems.

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Section: The Nf-κb Signaling Systemmentioning

confidence: 99%

Crosstalk via the NF-κB signaling system

Basak¹,

Hoffmann²

2008

Cytokine & Growth Factor Reviews

153

117

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“…Apart from I B␣, several other inhibitors for NF B (I B␤, I B⑀) have recently been cloned. 11 The relative contribution of these in controlling particularly chronic inflammation remains to be established.…”

Section: Figure 9 Emsa After Nf B Decoy Transfection (A) Cfte Cells mentioning

confidence: 99%

Anti-inflammatory gene therapy directed at the airway epithelium

Griesenbach¹,

Scheid²,

Hillery³

et al. 2000

Gene Ther

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“…p50 and p52 homodimers and p50/p52 heterodimers are able to translocate to the nucleus, but lack the NFkB transactivation domain and generally act as transcriptional repressors (8). IkBa inhibits p50 heterodimers containing cRel, RelA, and RelB (5,8,17), while IkBb preferentially inhibits RelA homo-and heterodimers (5,8,17,18) and IkBo is associated with cRel and RelA, but not p50 (5,19). NFkB binds to the promoters for p100/p52, p105/p50, and IkBa and transcriptionally activates their expression (8).…”

Section: Introductionmentioning

confidence: 99%

RelA, p50 and Inhibitor of kappa B alpha are Elevated in Human Metastatic Melanoma Cells and Respond Aberrantly to Ultraviolet Light B

McNulty

Tohidian

Meyskens

2001

Pigment Cell Research

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melanocytes. We also found that melanoma cells expressed Metastatic melanomas are typically resistant to radiation and chemotherapy. The underlying basis for this phenomenon may higher cytoplasmic levels of RelA, p105/p50 and the inhibitory protein, inhibitor of kappa B alpha (IkBa) than melanocytes. result in part from defects in apoptotic pathways. Nuclear factor kappa B (NFkB) has been shown to control apoptosis in To directly test whether RelA expression has an impact on melanoma cell survival, we used antisense RelA phosphorothmany cell types and normally functions as an immediate stress ioate oligonucleotides and found that melanoma cell viability response mechanism that is rigorously controlled by multiple inhibitory complexes. We have previously shown that NFkB was significantly decreased compared with untreated or conbinding is elevated in metastatic melanoma cells relative to trol cultures. The constitutive activation of NFkB in metastatic melanoma cell cultures may, therefore, support an normal melanocytes. In the current study, Western blot analysis showed that, compared with normal melanocytes, inappropriate cell survival pathway that can be therapeutically manipulated. melanoma cell lines have higher nuclear levels of the NFkB subunits p50 (7-fold) and RelA (5-10-fold). In response to Key words: Melanocyte, Melanoma, NFkB, Antisense, TNF, tumor necrosis factor-alpha (TNFa), both melanocytes and UVB melanoma cells showed increased nuclear p50 and RelA levels, but levels in melanoma cells remained higher than in Nuclear factor kappa B (NFkB) activation has been shown to have both pro-and anti-apoptotic functions in various cell types (5, 6). There are five mammalian NFkB/ Rel family members, p50, p52, RelA, RelB, and cRel, that share a highly conserved 300-amino acid Rel homology domain containing dimerization, nuclear localization, and DNA binding regions (5 -8). These proteins can form homoand heterodimers, which bind DNA at NFkB sequences found in the promoters of a variety of genes and specific dimer pairs elicit differential induction of these genes (5,8,9). Several studies have suggested that NFkB transcription

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I kappa B epsilon, a novel member of the Ikappa B family, controls RelA and cRel NF-kappa B activity

Cited by 367 publications

References 61 publications

Crosstalk via the NF-κB signaling system

Crosstalk via the NF-κB signaling system

Anti-inflammatory gene therapy directed at the airway epithelium

RelA, p50 and Inhibitor of kappa B alpha are Elevated in Human Metastatic Melanoma Cells and Respond Aberrantly to Ultraviolet Light B

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