ArticleNPJ genomic medicine2022
Ano5 modulates calcium signaling during bone homeostasis in gnathodiaphyseal dysplasia.
Article in NPJ genomic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Beyond osteopoikilosis: a blended skeletal dysplasia associated with dualJCEM case reports · 2026Article
- An alkaline nanosized platelet vesicle-based hydrogel for the treatment of osteoporotic bone defects.Materials today. Bio · 2026Article
- Genomic signatures of environmental adaptation in Danzhou chickens.BMC genomics · 2026Article
- Benign fibro-osseous lesions of the cranio-maxillofacial bones: an updated review with special emphasis on molecular pathogenesis.Journal of bone and mineral metabolism · 2026Review
- Anoctamin 5 mutation leads to abnormal bone homeostasis of GDD by regulating AMPK-dependent glucose metabolism.Frontiers in endocrinology · 2026Article
- ANO5 p.I616F variant drives florid cemento-osseous dysplasia by disrupting transmembrane domain structure.BMC oral health · 2025Article
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- Anoctamin-5 deficiency enhances ATG9A-dependent autophagy, inducing osteogenesis and gnathodiaphyseal dysplasia-like bone formation.JCI insight · 2025Article
- Ano5Bone reports · 2025Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
ANO5 encodes transmembrane protein 16E (TMEM16E), an intracellular calcium-activated chloride channel in the endoplasmic reticulum. Mutations in ANO5 are associated with gnathodiaphyseal dysplasia (GDD), a skeletal disorder causing the jaw deformity and long bone fractures. However, the coordinated mechanism by which ANO5 mediates bone homeostasis in GDD remains poorly defined. Here, we show that ablation of Ano5 reduced intracellular calcium transients, leading to defects in osteogenesis and osteoclastogenesis and thus bone dysplasia. We found a causative de novo ANO5 frameshift insertion mutation (p.L370_A371insDYWRLNSTCL) in a GDD family with osteopenia, accompanied by a decrease in TMEM16E expression and impaired RANKL-induced intracellular calcium ([Ca
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Registered trials
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