| First Author | Barro Soria R | Year | 2009 |
| Journal | J Biol Chem | Volume | 284 |
| Issue | 43 | Pages | 29405-12 |
| PubMed ID | 17003041 | Mgi Jnum | J:127210 |
| Mgi Id | MGI:3763330 | Doi | 10.1074/jbc.M605716200 |
| Citation | Barro Soria R, et al. (2009) Bestrophin-1 enables Ca2+-activated Cl- conductance in epithelia. J Biol Chem 284(43):29405-12 |
| abstractText | Epithelial cells express calcium-activated Cl(-) channels of unknown molecular identity. These Cl(-) channels play a central role in diseases such as secretory diarrhea, polycystic kidney disease, and cystic fibrosis. The family of bestrophins has been suggested to form calcium-activated Cl(-) channels. Here, we demonstrate molecular and functional expression of bestrophin-1 (BEST1) in mouse and human airways, colon, and kidney. Endogenous calcium-activated whole cell Cl(-) currents coincide with endogenous expression of the Vmd2 gene product BEST1 in murine and human epithelial cells, whereas calcium-activated Cl(-) currents are absent in epithelial tissues lacking BEST1 expression. Blocking expression of BEST1 with short interfering RNA or applying an anti-BEST1 antibody to a patch pipette suppressed ATP-induced whole cell Cl(-) currents. Calcium-dependent Cl(-) currents were activated by ATP in HEK293 cells expressing BEST1. Thus, BEST1 may form the Ca2+-activated Cl(-) current, or it may be a component of a Cl(-) channel complex in epithelial tissues. |
