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. 2011 Oct 31;32(Pt 2):105–112. doi: 10.1042/BSR20110089

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© 2012 The Author(s) The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Non-Commercial Licence (http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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(A) Normal transport of TNFR1 and (B) intracellular trafficking defects associated with TRAPS. TNFR1 is transported along the biosynthetic pathway through the ER to the Golgi storage pool, where the majority of the receptor is retained in cells of the immune system. TRAPS is thought to occur as a result of a number of possible mechanisms, namely defective TNFR1 oligomerization and ER misfolding-associated stress pathways, failed Golgi retention, impaired TNFR1 proteolytic cleavage and receptor shedding or ligand-independent NF-κB activation.