| http://purl.uniprot.org/citations/25899321 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25899321 | http://www.w3.org/2000/01/rdf-schema#comment | "Calcium-activated chloride channel (CaCC) plays an important role in modulating epithelial secretion. It has been suggested that in salivary tissues, sustained fluid secretion is dependent on Ca(2+) influx that activates ion channels such as CaCC to initiate Cl(-) efflux. However direct evidence as well as the molecular identity of the Ca(2+) channel responsible for activating CaCC in salivary tissues is not yet identified. Here we provide evidence that in human salivary cells, an outward rectifying Cl(-) current was activated by increasing [Ca(2+)]i, which was inhibited by the addition of pharmacological agents niflumic acid (NFA), an antagonist of CaCC, or T16Ainh-A01, a specific TMEM16a inhibitor. Addition of thapsigargin (Tg), that induces store-depletion and activates TRPC1-mediated Ca(2+) entry, potentiated the Cl(-) current, which was inhibited by the addition of a non-specific TRPC channel blocker SKF96365 or removal of external Ca(2+). Stimulation with Tg also increased plasma membrane expression of TMEM16a protein, which was also dependent on Ca(2+) entry. Importantly, in salivary cells, TRPC1 silencing, but not that of TRPC3, inhibited CaCC especially upon store depletion. Moreover, primary acinar cells isolated from submandibular gland also showed outward rectifying Cl(-) currents upon increasing [Ca(2+)]i. These Cl(-) currents were again potentiated with the addition of Tg, but inhibited in the presence of T16Ainh-A01. Finally, acinar cells isolated from the submandibular glands of TRPC1 knockout mice showed significant inhibition of the outward Cl(-) currents without decreasing TMEM16a expression. Together the data suggests that Ca(2+) entry via the TRPC1 channels is essential for the activation of CaCC."xsd:string |
| http://purl.uniprot.org/citations/25899321 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcp.25017"xsd:string |
| http://purl.uniprot.org/citations/25899321 | http://purl.uniprot.org/core/author | "Sun Y."xsd:string |
| http://purl.uniprot.org/citations/25899321 | http://purl.uniprot.org/core/author | "Birnbaumer L."xsd:string |
| http://purl.uniprot.org/citations/25899321 | http://purl.uniprot.org/core/author | "Singh B.B."xsd:string |
| http://purl.uniprot.org/citations/25899321 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/25899321 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/25899321 | http://purl.uniprot.org/core/pages | "2848-2856"xsd:string |
| http://purl.uniprot.org/citations/25899321 | http://purl.uniprot.org/core/title | "TRPC1 regulates calcium-activated chloride channels in salivary gland cells."xsd:string |
| http://purl.uniprot.org/citations/25899321 | http://purl.uniprot.org/core/volume | "230"xsd:string |
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