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    TRAF2 regulates TNF and NF-kappa B signalling to suppress apoptosis and skin inflammation independently of Sphingosine kinase 1

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    Author
    Etemadi, N; Chopin, M; Anderton, H; Tanzer, MC; Rickard, JA; Abeysekera, W; Hall, C; Spall, SK; Wang, B; Xiong, Y; ...
    Date
    2015-12-23
    Source Title
    eLife
    Publisher
    ELIFE SCIENCES PUBLICATIONS LTD
    University of Melbourne Author/s
    Nutt, Stephen; Vaux, David; Chopin, Michael; Anderton, Holly; Tanzer, Maria; Rickard, James; Smyth, Gordon; Nachbur, Ulrich; Silke, John; Ernst, Matthias
    Affiliation
    Medical Biology (W.E.H.I.)
    Surgery (RMH)
    School of Mathematics and Statistics
    Metadata
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    Document Type
    Journal Article
    Citations
    Etemadi, N., Chopin, M., Anderton, H., Tanzer, M. C., Rickard, J. A., Abeysekera, W., Hall, C., Spall, S. K., Wang, B., Xiong, Y., Hla, T., Pitson, S. M., Bonder, C. S., Wong, W. W. -L., Ernst, M., Smyth, G. K., Vaux, D. L., Nutt, S. L., Nachbur, U. & Silke, J. (2015). TRAF2 regulates TNF and NF-kappa B signalling to suppress apoptosis and skin inflammation independently of Sphingosine kinase 1. ELIFE, 4 (DECEMBER2015), https://doi.org/10.7554/eLife.10592.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258276
    DOI
    10.7554/eLife.10592
    Abstract
    TRAF2 is a component of TNF superfamily signalling complexes and plays an essential role in the regulation and homeostasis of immune cells. TRAF2 deficient mice die around birth, therefore its role in adult tissues is not well-explored. Furthermore, the role of the TRAF2 RING is controversial. It has been claimed that the atypical TRAF2 RING cannot function as a ubiquitin E3 ligase but counterclaimed that TRAF2 RING requires a co-factor, sphingosine-1-phosphate, that is generated by the enzyme sphingosine kinase 1, to function as an E3 ligase. Keratinocyte-specific deletion of Traf2, but not Sphk1 deficiency, disrupted TNF mediated NF-κB and MAP kinase signalling and caused epidermal hyperplasia and psoriatic skin inflammation. This inflammation was driven by TNF, cell death, non-canonical NF-κB and the adaptive immune system, and might therefore represent a clinically relevant model of psoriasis. TRAF2 therefore has essential tissue specific functions that do not overlap with those of Sphk1.

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