693
Views
0
CrossRef citations to date
0
Altmetric
Autophagic Punctum

Protein disorder in the regulatory control of mitophagy

& ORCID Icon
Article: 2242054 | Received 17 Jul 2023, Accepted 23 Jul 2023, Published online: 01 Aug 2023

Figures & data

Figure 1. Schema of the contributions of IDRs in the control of CLEC16A-RNF41-USP8 complex assembly. Stability of the CLEC16A-RNF41-USP8 complex is essential for optimal mitophagy. The CLEC16A C-terminal IDR increases CLEC16A stability by preventing degradative self-ubiquitination. CLEC16A stabilizes RNF41 via non-degradative ubiquitination, while RNF41 ubiquitinates and destabilizes CLEC16A by modifying the CLEC16A internal IDR. USP8 and RNF41 also participate in reciprocal cross-regulation. Overexpression of CLEC16A increases USP8 expression, yet the underlying mechanisms of this and the potential importance of the putative USP8 IDR in mitophagy remain unknown.

Figure 1. Schema of the contributions of IDRs in the control of CLEC16A-RNF41-USP8 complex assembly. Stability of the CLEC16A-RNF41-USP8 complex is essential for optimal mitophagy. The CLEC16A C-terminal IDR increases CLEC16A stability by preventing degradative self-ubiquitination. CLEC16A stabilizes RNF41 via non-degradative ubiquitination, while RNF41 ubiquitinates and destabilizes CLEC16A by modifying the CLEC16A internal IDR. USP8 and RNF41 also participate in reciprocal cross-regulation. Overexpression of CLEC16A increases USP8 expression, yet the underlying mechanisms of this and the potential importance of the putative USP8 IDR in mitophagy remain unknown.