Transmembrane protein that binds to and facilitates the assembly of lysosomal proton-transporting V-type ATPase (v-ATPase), resulting in enhanced lysosomal acidification and trafficking (By similarity). By bringing the v-ATPase accessory protein ATP6AP2 and the v-ATPase subunit ATP6V0D1 together, allows v-ATPase complex formation and activation (By similarity). TMEM9-controlled vesicular acidification induces hyperactivation of Wnt/beta-catenin signaling, involved in development, tissue homeostasis and tissue regeneration, through lysosomal degradation of adenomatous polyposis coli/APC (PubMed:30374053, PubMed:32380568). In the liver, involved in hepatic regeneration (PubMed:32380568). Interacts with the v-ATPase accessory protein ATP6AP2 and with the v-ATPase complex subunit ATP6V0D1; these interactions lead to the assembly of the v-ATPase complex. Expressed in heart, lung, kidney, liver and intestines (PubMed:30374053). Enriched in the hepatocytes around the central vein (PubMed:32380568). The transmembrane domain (TMD) is essential for the interaction with ATP6AP2. N-glycosylated. Knockout mice are viable and exhibit no discernible phenotypes in the overall liver architecture and hepatocytes (PubMed:30374053, PubMed:32380568). However, they display impaired hepatic regeneration with reduced Wnt signaling (PubMed:32380568). Knockout mice also show a suppression of intestinal tumorigenesis (PubMed:30374053). Belongs to the TMEM9 family.