Slo2b
Description: potassium channel, subfamily T, member 2 Gene: Kcnt2 Alias: Slo2b, kcnt2, KNa1.2, KCa4.2, Slo2.1
KNa channels were first identified in guinea pig cardiomyocytes (Kameyama et al., 1984 [1149]). Subsequently, similar channels were reported in a variety of neurons (Bader et al., 1985 [1150]; Dryer et al., 1989 [1151]; Schwindt et al., 1989 [1152]; Dryer, 1991 [1145]; Egan et al., 1992a [1153]; Haimann et al., 1992 [1143]; Dale, 1993 [13; Safronov and Vogel, 1996 [1155]; Bischoff et al., 1998 [1144]). Like Ca2+ -activated BK and SK channels, the properties of KNa channels appear to be diverse. The reported unitary conductances of these channels range from 105 to 200 pS, and half-maximal activation by Na+ occurs between 7 and 80 mM, depending on cell type and recording conditions (Dryer, 1994 [1148]).
KCNT2 (also known as SLICK; KCa4.2; SLO2.1; MGC119610; MGC119611; MGC119612; MGC119613; RP11-58O13.1) encodes Slo2b, a potassium channel, subfamily T, member 2.
http://www.ncbi.nlm.nih.gov/gene/343450
Transcript
| Species | NCBI accession | Length (nt) | |
|---|---|---|---|
| Human | NM_198503.5 | 5984 | |
| Mouse | NM_001081027.3 | 8280 | |
| Rat | NM_198762.2 | 3845 |
Protein Isoforms
Isoforms
Post-Translational Modifications
Structure
Slo2b predicted AlphaFold size
Methodology for AlphaFold size prediction and disclaimer are available here
With similar single-channel conductance to Slack, Slick also rectifies outwardly and is activated by intracellular Na+. In marked contrast to Slack, however, Slick activation occurs very rapidly with step changes in voltage, whereas Slack activation increases with time after a step depolarization. (Bhattacharjee [1141])
Slick (Slo2.1) is selectively expressed in the nervous system and heart. (Bhattacharjee [1141])
The physiological roles of KNa channels (such as Slo2b) appear to be distinct in different cell types. For example, in quail trigeminal ganglion neurons and in dorsal root ganglion neurons, it has been suggested that KNa channels regulate the resting membrane potential (Haimann et al., 1992 [1143]; Bischoff et al., 1998 [1144]). In other neurons, KNa channels have been implicated in an apamin-insensitive, Na+-dependent slow afterhyperpolarization (AHP) that follows a burst of action potentials (Dryer, 1994 [1145]). In ferret perigeniculate neurons, such a Na+-dependent slow AHP is an important component of spindle wave activity (Kim and McCormick, 1998 [1146]). It has also been proposed that KNa channels may be activated by a single action potential and may therefore play a role in determining the duration of action potentials (Bertrand et al., 1989 [1147]), although is unclear whether the amount of Na+ influx through a TTX-sensitive Na+ channel during a single action potential is normally sufficient to activate KNa channels (Dryer, 1994 [1148], 1991 [1145]). Activation may depend on the relative rates of influx, diffusion, and extrusion of Na+, the proximity of KNa channels to the source of Na+, and the particular geometry of the space occupied by KNa channels in a given cell type (Dryer, 1994 [1148], 1991 [1145]).
The properties of the Slick channel indicate that its activation by intense neuronal activity or by hypoxia may hyperpolarize specific neurons in the brain and the heart, where the channel is expressed, thereby limiting excitability and energy consumption to maintain cell viability. (Bhattacharjee [1141])
The activity of Slick channels is substantially more sensitive than Slack to changes in intracellular Cl-, and Slick open probability is significant even in the absence of Na+. Moreover, Slick contains a regulatory nucleotidebinding site that is responsible for ATP-dependent inhibition of channel activity. (Bhattacharjee [1141])
References
Bhattacharjee A
et al.
Slick (Slo2.1), a rapidly-gating sodium-activated potassium channel inhibited by ATP.
J. Neurosci.,
2003
Dec
17
, 23 (11681-91).
Haimann C
et al.
Sodium-activated potassium current in sensory neurons: a comparison of cell-attached and cell-free single-channel activities.
Pflugers Arch.,
1992
Dec
, 422 (287-94).
Bischoff U
et al.
Na+-activated K+ channels in small dorsal root ganglion neurones of rat.
J. Physiol. (Lond.),
1998
Aug
1
, 510 ( Pt 3) (743-54).
Dryer SE
Na(+)-activated K+ channels and voltage-evoked ionic currents in brain stem and parasympathetic neurones of the chick.
J. Physiol. (Lond.),
1991
Apr
, 435 (513-32).
Kim U
et al.
Functional and ionic properties of a slow afterhyperpolarization in ferret perigeniculate neurons in vitro.
J. Neurophysiol.,
1998
Sep
, 80 (1222-35).
Bertrand D
et al.
KNa. A sodium-activated potassium current.
Pflugers Arch.,
1989
, 414 Suppl 1 (S76-9).
Dryer SE
Na(+)-activated K+ channels: a new family of large-conductance ion channels.
Trends Neurosci.,
1994
Apr
, 17 (155-60).
Kameyama M
et al.
Intracellular Na+ activates a K+ channel in mammalian cardiac cells.
Nature,
1984 May 24-30
, 309 (354-6).
Bader CR
et al.
Sodium-activated potassium current in cultured avian neurones.
Nature,
1985 Oct 10-16
, 317 (540-2).
Dryer SE
et al.
A Na+-activated K+ current in cultured brain stem neurones from chicks.
J. Physiol. (Lond.),
1989
Mar
, 410 (283-96).
Schwindt PC
et al.
Long-lasting reduction of excitability by a sodium-dependent potassium current in cat neocortical neurons.
J. Neurophysiol.,
1989
Feb
, 61 (233-44).
Egan TM
et al.
Properties and rundown of sodium-activated potassium channels in rat olfactory bulb neurons.
J. Neurosci.,
1992
May
, 12 (1964-76).
Dale N
A large, sustained Na(+)- and voltage-dependent K+ current in spinal neurons of the frog embryo.
J. Physiol. (Lond.),
1993
Mar
, 462 (349-72).
Safronov BV
et al.
Properties and functions of Na(+)-activated K+ channels in the soma of rat motoneurones.
J. Physiol. (Lond.),
1996
Dec
15
, 497 ( Pt 3) (727-34).
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