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Adaptophagy

This term has been proposed by Till et al (2013) for the selective degradation of signaling adaptors downstream of Toll-like receptors (such as TLR3) or similar types of receptor families. Ellinghaus et al (2013) have reported mutations in NDP52 that impair the regulatory functions of NDP52 to inhibit NF-kappa-B activation of genes regulating inflammation and affecting the stability of proteins in Toll-like receptor pathways. NDP52 is an adaptor protein that functions in selective autophagy of intracellular bacteria and signaling molecules, which appears to support a role of autophagy in the pathogenesis of Crohn's diserase.

For a related term pertaining to the degradation of signaling molecules see also: Signalphagy.

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