Snx18, a member of the sorting nexin (SNX) protein family, contains a Phox homology (PX) domain. It is involved in multiple cellular processes such as membrane remodeling, endocytic trafficking, and autophagosome biogenesis [3,4,6]. These functions are crucial for maintaining normal cellular homeostasis, and its role in autophagy suggests implications in cell survival and stress response pathways [1,6]. Genetic models can be valuable in further elucidating its functions.

In autophagosome biogenesis, Snx18 acts as a positive regulator. It interacts with ATG16L1 and LC3, functioning downstream of ATG14 and the class III PtdIns3K complex. It promotes LC3 lipidation and tubulation of recycling endosomes, providing membrane for phagophore expansion [1,6]. In ATG9A trafficking, Snx18 recruits Dynamin-2 to regulate the trafficking of ATG9A from recycling endosomes, which is important for autophagosome precursor membrane formation [2]. In endocytic trafficking, Snx18 has a redundant role with Snx9 at the plasma membrane, interacting with dynamin, N-WASP, and synaptojanin, and its depletion inhibits transferrin uptake [3]. It also plays a role in mitosis, as depletion of Snx18 using siRNA induces multinucleation and an accumulation of cytokinetic cells, disrupting MRLC(S19) localization and Rab11-positive recycling endosome recruitment during cytokinesis [5].

In summary, Snx18 is essential for processes like autophagosome biogenesis, endocytic trafficking, and mitosis. Although no disease-specific implications from KO/CKO mouse models are given in the provided references, understanding its functions through such models can potentially offer insights into diseases related to disrupted autophagy, endocytosis, or cell division processes.