CFTR |
CFTR, P13569
|
apigenin (Potentiation), capsaicin (Potentiation), CBIQ (Potentiation), felodipine (Potentiation), genistein (Potentiation), nimodipine (Potentiation), NS004 (Potentiation), phenylglycine-01 (Potentiation), SF-01 (Potentiation), UCCF-029 (Potentiation), UCCF-339 (Potentiation), UCCF-853 (Potentiation), VX-770 (Potentiation) |
intracellular CFTRinh-172 (intracellular application prolongs mean closed time), GaTx1, glibenclamide, extracellular GlyH-101 |
γ = 6–10 pS; permeability sequence = Br- ≥ Cl- > I- > F-, (PI/PCl = 0.1–0.85); slight outward rectification; phosphorylation necessary for activation by ATP binding at binding nucleotide binding domains (NBD)1 and 2; positively regulated by PKC and PKGII (tissue specific); regulated by several interacting proteins including syntaxin 1A, Munc18 and PDZ domain proteins such as NHERF (EBP50) and CAP70 |
UCCF-339, UCCF-029, apigenin and genistein are examples of flavones. UCCF-853 and NS004 are examples of benzimidazolones. CBIQ is an example of a benzoquinoline. felodipine and nimodipine are examples of 1,4-dihydropyridines. phenylglycine-01 is an example of a phenylglycine. SF-01 is an example of a sulfonamide. Malonic acid hydrazide conjugates are also CFTR channel blockers (see Verkman and Galietta, 135
155) |