Overview
- Peptide RQVRLKHRKLREQV(C), corresponding to amino acid residues 350-363 of rat KCNN4 (Accession Q9QYW1). Intracellular, C-terminal part.
- KCa3.1-transfected HEK-293 and K562 (Human chronic myelogenous leukemia) cells (1:300).
Western blot analysis of KCa3.1-transfected HEK-293 (lanes 1 and 3) and Human K562 chronic myelogenous leukemia (lanes 2 and 4) cells:1,2. Anti-KCNN4 (KCa3.1, SK4) Antibody (#APC-064), (1:200).
3,4. Anti-KCNN4 (KCa3.1, SK4) Antibody, preincubated with KCNN4/KCa3.1 Blocking Peptide (#BLP-PC064).
- Human bronchial epithelial NuLi cells (1:100) (Klein, H. et al. (2009) Am. J. Physiol. Cell Physiol. 296, C285.).
- Normal rat cholangiocytes (NRC) (1:200) (Dutta, A.K. et al. (2009) Am. J. Physiol. Gastrointest. Liver Physiol. 297, G1009.).
KCa3.1 (KCNN4, SK4) is a member of the Ca2+ activated K+ channel family that shares the characteristic of being activated by intracellular Ca2+. The channel has an intermediate conductance, is voltage insensitive and is activated by Ca2+ in the submicromolar range. The channel has a similar topology to that of KV channels, that is, six transmembrane domains and intracellular N- and C-termini.
KCa3.1 is widely expressed in epithelial, endothelial and cells of hematopoietic origin. In erythrocytes (red blood cells) it has been identified as the molecular correlate of the so-called Gardos channel.
The functional role of the channel is to set the cell membrane potential at negative values so as to aid in the electrochemical transport of other ions such as Cl- and Ca2+. Indeed, KCa3.1 has a key role in sustaining the Ca2+ influx in activated T lymphocytes and in regulating Cl- secretion from colon epithelium. Therefore, specific blockers of the KCa3.1 channel have been proposed for the treatment of several diseases including autoimmune diseases, secretory diarrhea and sickle cell anemia.
