sub:provenance {
  beldoc: dce:description "Approximately 61,000 statements." ;
    dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved." ;
    dce:title "BEL Framework Large Corpus Document" ;
    pav:authoredBy sub:_4 ;
    pav:version "20131211" .
  sub:_3 prov:value "At the molecular level, all cardiac Cl? channels described so far may fall into the following Cl? channel gene families: (1) the cystic fibrosis transmembrane conductance regulator (CFTR), which is a member of the adenosine triphosphate-binding cassette (ABC) transporter superfamily and may be responsible for the Cl? currents activated by protein kinase A (PKA) (I Cl,PKA), protein kinase C (PKC) (I Cl,PKC) , and extracellular ATP (I Cl,ATP) in the heart; (2) ClC-2, which is a member of the ClC voltage-gated Cl? channel superfamily and may be responsible for the hyperpolarization- and cell swelling-activated inwardly rectifying Cl? current (I Cl,ir) (Duan et al. 2000; Komukai C   et al. 2002a,b); (3) ClC-3, which is also a member of the ClC voltage-gated Cl? channel superfamily and may be responsible for the volume-regulated outwardly rectifying Cl? current (I Cl,vol), including the basally activated (I Cl,b) and swelling activated (I Cl,swell) components; (4) CLCA-1, which was thought to be responsible for the Ca2+-activated Cl? current (I Cl,Ca); (5) Bestrophin, a candidate also for I Cl,Ca; and (6) TMEM16, a novel candidate for I Cl,Ca " ;
    prov:wasQuotedFrom pubmed:19171656 .
  sub:_4 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:19171656 ;
    prov:wasDerivedFrom beldoc: , sub:_3 .
}