Mechanism of hypoxia-induced NFκB

Andrew Melvin, Sharon Mudie, Sonia Rocha (Lead / Corresponding author)

    Research output: Contribution to journalArticlepeer-review

    37 Citations (Scopus)


    The cellular response to hypoxia relies on the activation of a specific transcriptional program. Although, most of the attention is focused on the transcription factor HIF, other transcription factors are also activated in hypoxia. We have recently described the mechanism for hypoxia induced NF kappa B. We have demonstrated the crucial dependency on the IKK complex as well as in the upstream IKK kinase TAK1. TAK1 and IKK activation is dependent upon the calcium calmodulin kinase, CaMK2 and requires Ubc13 as the E2 ubiquitin conjugation enzyme. We report a role for XIAP as the possible E3-ubiquitin ligase for this system. Interestingly, hypoxia induced IKK mediated phosphorylation of I kappa B alpha, does not lead to degradation. Hypoxia prevents I kappa B alpha de-sumoylation of Sumo-2/3 chains on critical lysine residues, normally required for K-48 linked polyubiquitination. Our results define a novel pathway regulating NF kappa B activation.

    Original languageEnglish
    Pages (from-to)879-882
    Number of pages4
    JournalCell Cycle
    Issue number6
    Publication statusPublished - 2011


    • hypoxia
    • NFkappaB
    • IKK
    • TAK1
    • XIAP
    • sumo
    • senps


    Dive into the research topics of 'Mechanism of hypoxia-induced NFκB'. Together they form a unique fingerprint.

    Cite this