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Outward rectifying potassium channel. Additionally we are shipping and many more products for this protein.
Showing 10 out of 81 products:
Human Polyclonal KCNT2 Primary Antibody for EIA, FACS - ABIN953018
Santi, Ferreira, Yang, Gazula, Butler, Wei, Kaczmarek, Salkoff: Opposite regulation of Slick and Slack K+ channels by neuromodulators. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2006
Show all 3 references for ABIN953018
Human Monoclonal KCNT2 Primary Antibody for ICC, IF - ABIN863117
Bhattacharjee, Joiner, Wu, Yang, Sigworth, Kaczmarek: Slick (Slo2.1), a rapidly-gating sodium-activated potassium channel inhibited by ATP. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2003
Show all 2 references for ABIN863117
KCNT2 SNPs were associated with lifetime cannabis use, but the association did not reach genome-wide significance. [Meta-Analysis]
Together these results suggest that hydrophobic interactions between residues in S5 and the C-terminal end of the pore helix stabilize Slo2.1 channels in a closed state.
Charge reversal of Asp757 of Slo2.1 prevented activation of channels by intracellular Na+, whereas activation by niflumic acid was unaffected.
Slick channels, in contrast to the similar Slack (show KCNT1 Antibodies) channels, are the only high-conductance K+ channels strongly sensitive to small changes in cell volume.
Together these findings suggest that (1) the selectivity filter and not the bundle crossing gates ion permeation and (2) dynamic coupling between the pore helix and the S5 and S6 segments mediates Slo2.1 channel activation.
Cloning and regulation of slick channel activity.
Slick (Slo2.1 (show KCNT1 Antibodies)) is required for both volatile anesthetics-stimulated K flux and for the anesthetic preconditioning-induced cardioprotection
Slick and Slack (show KCNT1 Antibodies) are expressed at high levels auditory brainstem. Activation of these KNa channels allows temporal accuracy of firing to be increased at high frequencies of stimulation.
Outward rectifying potassium channel. Produces rapidly activating outward rectifier K(+) currents. Activated by high intracellular sodium and chloride levels. Channel activity is inhibited by ATP and by inhalation anesthetics, such as isoflurane (By similarity). Inhibited upon stimulation of G-protein coupled receptors, such as CHRM1 and GRIA1.
potassium channel, subfamily T, member 2
, potassium channel subfamily T member 2-like
, potassium channel subfamily T member 2
, sequence like an intermediate conductance potassium channel subunit
, sodium activated potassium channel
, sodium and chloride activated ATP sensitive potassium channel
, sodium and chloride-activated ATP-sensitive potassium channel Slo2.1
, sodium- and chloride-activated ATP-sensitive potassium channel
, sodium-and chloride-activated ATP-sensitive potassium channel (SLICK)
, sodium- and chloride-activated ATP-sensitive potassium channel subunit