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It is highly expressed in bone and the gut where it participates in bone mineral and calcium homeostasis through the regulation of osteoclastic bone resorption and gastric acid secretion, respectively. Not surprisingly, patients harboring mutations in SNX10 mutation manifest a phenotype of autosomal recessive osteopetrosis or malignant infantile osteopetrosis, which is clinically characterized by dense bones with increased cortical bone into the medullary space with bone marrow occlusion or depletion, bone marrow failure, and anemia. Accordingly, SNX10 mutant osteoclasts exhibit impaired bone resorptive capacity. Beyond the skeleton, there is emerging evidence implicating SNX10 in cancer development, metabolic disorders, inflammation, and chaperone\u2010mediated autophagy. Understanding the structural basis through which SNX10 exerts its diverse biological functions in both cell and tissue\u2010specific manners may therefore inform new therapeutic opportunities toward\u00a0the treatment and management of SNX10\u2010related diseases.<\/jats:p>","DOI":"10.1002\/jcp.30173","type":"journal-article","created":{"date-parts":[[2020,11,26]],"date-time":"2020-11-26T04:28:43Z","timestamp":1606364923000},"page":"4207-4215","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["The molecular structure and function of sorting nexin 10 in skeletal disorders, cancers, and other pathological conditions"],"prefix":"10.1002","volume":"236","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2021-8309","authenticated-orcid":false,"given":"Jiake","family":"Xu","sequence":"first","affiliation":[{"name":"Division of Regenerative Biology, School of Biomedical Sciences University of Western Australia  Perth 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