FIP200 (RB1CC1) is a critical regulator of canonical macroautophagy and has also emerged as a crucial regulator of selective autophagy as well as inflammatory processes. The illumination of FIP200's role in autophagy at the molecular level has been accompanied by studies demonstrating the importance of its autophagy function in physiological processes in mammals and pathological contexts such as cancer. However, there is an increasing appreciation that most, if not all of the autophagy genes, also play a role in other processes such as LC3-associated phagocytosis, vesicle trafficking and protein secretion. Consequently, this has led to efforts in generating specific mutants of autophagy genes that are more amenable to dissecting their autophagy versus non-autophagy functions. In this aspect, we have generated a FIP200 knock-in mouse allele that is defective for canonical macroautophagy. This has revealed a canonical-autophagy-independent function of FIP200 that is responsible for limiting pro-inflammatory signaling. In this review, we will discuss FIP200's role in this process, the implications with regards to cancer immunotherapy and highlight key prospective avenues to specifically dissect the distinct functions of FIP200.
Review Article| July 14 2020
Role of FIP200 in inflammatory processes beyond its canonical autophagy function
Syn Kok Yeo;
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Syn Kok Yeo, Chenran Wang, Jun-Lin Guan; Role of FIP200 in inflammatory processes beyond its canonical autophagy function. Biochem Soc Trans 28 August 2020; 48 (4): 1599–1607. doi: https://doi.org/10.1042/BST20191156
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