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Validated All-in-One™ qPCR Primer for KCNN2(NM_170775.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
Action potentials in vertebrate neurons are followed by an afterhyperpolarization (AHP) that may persist for several seconds and may have profound consequences for the firing pattern of the neuron. Each component of the AHP is kinetically distinct and is mediated by different calcium-activated potassium channels. The protein encoded by this gene is activated before membrane hyperpolarization and is thought to regulate neuronal excitability by contributing to the slow component of synaptic AHP. The encoded protein is an integral membrane protein that forms a voltage-independent calcium-activated channel with three other calmodulin-binding subunits. This gene is a member of the KCNN family of potassium channel genes. Two transcript variants encoding different isoforms have been found for this gene.
Gene References into function
- RT-PCR analysis showed strong expression of SK2 mRNA in the normal human colon.
- Because of the marked differential expression of SK2 channels in the heart, specific ligands for Ca2+-activated K+ currents may offer a unique therapeutic opportunity to modify atrial cells without interfering with ventricular myocytes
- SK2 plays an important role in mediating the increase in transepithelial secretion due to increases in intracellular Ca 2+. SK2 channels, therefore, may represent a target for pharmacologic modulation of bile flow.
- The subtype SK2 channels were up-regulated under hypoxia, shown with pharmacological tools and with mRNA analysis.
- Functions of SK2 channels in atrial myocytes are critically dependent on the normal expression of Ca(v)1.3 Ca(2+) channels.
- Results suggest that SK2-channel activation may largely contribute to the sustained Ca2+ influx in the G0/G1 phase in comparison of that in the G2/M phase in Jurkat T-lymphocytes.