anti-Potassium Voltage-Gated Channel, Shaw-Related Subfamily, Member 1 (KCNC1) Antibodies

Mouse (Murine) Potassium Voltage-Gated Channel, Shaw-Related Subfamily, Member 1 (KCNC1) interaction partners

1. Kv3.1 channels stimulate adult neural precursor cell proliferation and neuronal differentiation.

2. The resting (closed) Kv3.1 channel conformation forms the high-affinity state for gambierol.

3. high-affinity multimeric binding between the Kv3.1 T1 domain and KIF5B requires three basic residues in the KIF5B tail. Kv3.1 T1 competes with the motor domain and microtubules, but not with kinesin light chain 1 (KLC1), for binding to the KIF5B tail.

4. Although all Kv3 transcripts were significantly expressed at embryonic age in whole brain extracts, only Kv3.1, Kv3.2 and Kv3.4 subunit proteins were present, suggesting a novel role for Kv3 channels at this developmental stage.

5. Block of Kv3.1 channels hinders spike repolarization and severely depresses evoked fast firing in deep cerebellar nuclear neurons.

6. Mice lacking both Kcnc1 and Kcnc2 genes fail to express the Kv3.1 and Kv3.2 channels in in the suprachiasmatic nucleus.

7. These results provide evidence that acoustically driven auditory activity can selectively regulate high-threshold potassium currents in the MNTB of normal hearing mice, likely due to an increased membrane expression of Kv3.1b channels.

8. As Kcnc1, but not Kcnc3, alleles are lost, mutant mice exhibit increasing gait ataxia accompanied by spike broadening and deceleration in deep cerebellar nuclei. neurons.

9. interaction with CALP/KCHIP4

10. NCS-1 is an accessory subunit of Kv4-encoded I(to,f) channels that functions to regulate I(to,f) density in the mammalian myocardium.

11. Kv4.3, in association with K(+) channel-interacting proteins, is the major molecular determinant of A-type potassium current in murine colonic myocytes.

12. Modulation of the kv3.1b potassium channel isoform adjusts the fidelity of the firing pattern of auditory neurons.

13. Motor deficits and altered synaptic transmission at the parallel fiber-Purkinje cell synapse in Kv3.1 knockout mice.

14. Ongoing activity in auditory brainstem neurons is necessary for the maintenance of Kv3.1 tonotopicity through the CREB pathway

15. Double mutant Kv3.1/Kv3.3-deficient mice are constitutively hyperactive. Increased ambulatory and stereotypic activity in conjunction with sleep loss was seen in Kv3.1-single mutants but not in Kv3.3-single mutants.

16. Starburst amacrine cells have large outward currents which are mediated in part by the Kv3.1 channel.

17. all Renshaw cells expressed Kv3.1b weakly from postnatal day 14, and strongly at postnatal day 21.

18. two voltage-gated potassium channels, Kv3.1 and Kv3.3, control sleep in wild-type and Kv3-mutant mice

19. Calcineurin and NFATc3 constitute a Ca(2+)-driven signaling module that contributes to the nonuniform distribution of Kv4 expression, and hence Ito function, in the mouse left ventricle.

20. K(V)3.1 K(+) current accounts for significant component of total K(+) current in oligodendrocyte lineage and, in association with OSP/claudin-11, plays significant role in OPC proliferation and migration and myelination of axons.

Human Potassium Voltage-Gated Channel, Shaw-Related Subfamily, Member 1 (KCNC1) interaction partners

1. A recurrent de novo mutation in KCNC1 (c.959G>A, p.Arg320His) has been identified recently as one of the important genetic causes of progress myoclonic epilepsy. This recurrent mutation in KCNC1 was identified in the two brothers who showed characteristic features of myoclonus epilepsy and ataxia due to potassium channel mutation (MEAK). The asymptomatic mother was suspected as being mosaic for this mutation.

2. KNCN1 p.R320H mutation causes MEAK syndrome.

3. A nonsense variant in KCNC1 gene was identified in three family members with intellectual disability without seizures.

4. reviews the phenotype/genotype of progressive myoclonus epilepsy and ataxia due to potassium channel mutation (MEAK)associated with KCNC1 mutations [review]

5. KCNC1 produces a resurgent current during repolarization, ensuring enough repolarizing power to terminate each action potential. The current results from a combination of steep voltage-dependent gating kinetics and ultra-fast voltage-sensor relaxation.

6. A recurrent KCNC1 de novo mutation, c.959G>A (p.Arg320His), is a new major cause for progressive myoclonus epilepsy. It has a dominant-negative loss-of-function effect.

7. Findings show a decrease in Kv3.1b channel protein in schizophrenia neocortex, a deficit that is restored by antipsychotic drugs

8. Describes localization in mouse brain of two isoforms - the longer is called b and the shorter is called a.

9. Describes two rat isoforms of Kv3.1, alpha is the longer one and beta is the shorter one

10. KChIP4a suppresses A-type Kv4 current via ER retention and enhancement of Kv4 closed-state inactivation.

11. Although all KV3 subunit transcripts are significantly expressed at embryonic age in whole mouse brain extracts, only KV3.1, KV3.2 and KV3.4 subunit transgenic proteins are present.

12. demonstrated that glycosylation was necessary for both DPP10 trafficking to the cell surface and functional interaction with Kv4 channels

13. Kv3.1 channels are transported into axons by binding to kinesin I.

14. In the absence of potassium ion, significant N-methyl-D-glucamine (NMDG)-positive currents could be recorded from human embryonic kidney cells expressing Kv3.1 or Kv3.2b channels and Kv1.5 Arg487Tyr/Val, but not wild-type channels.