| First Author | Wanitchakool P | Year | 2017 |
| Journal | Cell Signal | Volume | 30 |
| Pages | 41-49 | PubMed ID | 27838374 |
| Mgi Jnum | J:322954 | Mgi Id | MGI:6869262 |
| Doi | 10.1016/j.cellsig.2016.11.006 | Citation | Wanitchakool P, et al. (2017) Cellular defects by deletion of ANO10 are due to deregulated local calcium signaling. Cell Signal 30:41-49 |
| abstractText | TMEM16K (ANO10) belongs to a family of ion channels and phospholipid scramblases. Mutations in ANO10 cause neurological and immunological defects, and abrogated ion transport. Here we show that Ano10 knockout in epithelial cells leads to defective ion transport, attenuated volume regulation and deranged Ca(2+) signaling. Intestinal epithelial cells from Ano10 null mice are reduced in size and demonstrate an almost abolished spontaneous and TNFalpha-induced apoptosis. Similar defects were found in mouse peritoneal Ano10 null macrophages and in human THP1 macrophages with reduced ANO10 expression. A cell cycle dependent colocalization of Ano10 with acetylated tubulin, centrioles, and a submembranous tubulin containing compartment was observed in Fisher rat thyroid cells. Axs, the Drosophila ortholog of ANO10 is known for its role in mitotic spindle formation and association with the endoplasmic reticulum and Ca(2+) signaling. We therefore propose that mutations in ANO10 cause cellular defects and genetic disorders through deranged local Ca(2+) signaling. |
