Mechanism of von Hippel-Lindau Protein-Mediated Suppression of Nuclear Factor kappa B Activity

An, Jiabin; Rettig, Matthew B.

doi:10.1128/mcb.25.17.7546-7556.2005

Cited by 102 publications

(90 citation statements)

References 54 publications

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“…3A). Because VBP1 has been reported to interact with VHL directly, we speculated that the regulatory effect of VBP1 on the NFκB activity might be related to VHLmediated NFκB regulation (28). As previously reported (28), we confirmed that the NFκB activity was repressed by VHL (Fig.…”

Section: Vbp1 Enhances Hbx-mediated Nfκb Activationsupporting

confidence: 78%

“…Interestingly, VHL binding protein (VBP1) which is interacting with von Hippel-Lindau protein (VHL) was identified that binds to HBx. Recently it has been reported that VHL is associated with the regulation of NFκB (28). Therefore, we could easily speculate that VBP1 might be involved in the regulatory mechanism of HBx in the activation of NFκB.…”

Section: Introductionmentioning

confidence: 99%

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Hepatitis B virus X protein enhances NFκB activity through cooperating with VBP1

Kim

Kim²,

Kim³

et al. 2008

BMB Reports

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Section: Vbp1 Enhances Hbx-mediated Nfκb Activationsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Hepatitis B virus X protein enhances NFκB activity through cooperating with VBP1

Kim

Kim²,

Kim³

et al. 2008

BMB Reports

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“…These data suggest the intriguing possibility that hypoxia increases IKK stability through an inhibition of protein hydroxylation, resulting in evasion of degradation in a similar manner to HIF-1. Indeed, it is worth noting that a number of studies have demonstrated that the E3 pVHL suppresses NF B activity in normoxia (30)(31)(32). However, although IKK␤ interacts with VHL in normoxia, we found no evidence for its ubiquitination/degradation.…”

Section: Resultsmentioning

confidence: 99%

Prolyl hydroxylase-1 negatively regulates IκB kinase-β, giving insight into hypoxia-induced NFκB activity

Cummins

Berra

Comerford

et al. 2006

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

713

599

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“…VHL promotes K48 ubiquitination of HIF-α subunits in normoxia 25 . VHL has also been shown to negatively regulate NF-κB activity 33 and HIFindependent mechanisms have been put forward 34 . With further research being conducted, it is very likely that additional common regulators will be identified.…”

Section: Hif and Nf-κb Functional Crosstalk Shared Targets And Activmentioning

confidence: 99%

A tale of two transcription factors: NF-kB and HIF crosstalk

Bandarra¹,

Rocha²

2013

OA Molecular and Cell Biology

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Introduction Hypoxia-inducible factor is a key transcriptional factor involved in the cellular response to low levels of oxygen, hypoxia. Moreover, hypoxiainducible factor has been recently associated with a role in inflammation and immunity. Importantly, hypoxiainducible factor is regulated by the major inflammatory responsive transcription factor, nuclear factor-κB. These two major pathways have been intimately linked. On one hand, they share a number of common target genes; on the other hand, physical interactions between hypoxiainducible factor subunits and nuclear factor-κB have been observed. Even though the role of nuclear factor-κB over hypoxia-inducible factor is fairly well-known, the involvement of hypoxia-inducible factor over the nuclear factor-κB pathway is not. Given the overlap between these pathways, it would not be surprising to find a functional involvement of hypoxiainducible factor in processes where nuclear factor-κB is involved. In this review, we will describe the communalities between hypoxia-inducible factor and nuclear factor-κB pathways, highlighting the crosstalk that occurs in a variety of conditions. Conclusion Taken together all the communalities between hypoxia-inducible factor and nuclear factor-κB pathways, there is no doubt that a cross-

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Mechanism of von Hippel-Lindau Protein-Mediated Suppression of Nuclear Factor kappa B Activity

Cited by 102 publications

References 54 publications

Hepatitis B virus X protein enhances NFκB activity through cooperating with VBP1

Hepatitis B virus X protein enhances NFκB activity through cooperating with VBP1

Prolyl hydroxylase-1 negatively regulates IκB kinase-β, giving insight into hypoxia-induced NFκB activity

A tale of two transcription factors: NF-kB and HIF crosstalk

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