Abstract
Background: TNF receptor I (TNFR1) recruits TNF Receptor-associated death domain (TRADD) and multiple kinases that ultimately phosphorylate inhibitor kappa B (IkBa). Subsequent degradation of phospho-IkBa (p-IkBa) frees nuclear factor kappa B (NF-kB) so it may be phosphorylated and made active. Many receptors require clathrin-mediated endocytosis to provide the scaffolds necessary for signaling to proceed. Therefore, we investigated the role of clathrin heavy chain (CHC) in TNFa-induced IkBa phosphorylation and NF-kB activation.
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