Abstract
A paper by Sun et al. identified the Ca2+-activated Cl− channel anoctamin 1 or ANO1 (TMEM16A) as an important regulator of osteoclast function by interacting with RANKL activating signaling pathways involved in bone resorption. Although Cl− transporters (e.g. ClC7, CLIC5) have been known to be involved in the active process of bone resorption, ANO1 appears to control osteoclast differentiation and function to levels beyond those of other Cl−transporters. Regulating ANO1 function might be a useful target for therapeutics in osteoporosis.
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