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The Shaker gene family of Drosophila encodes components of voltage-gated potassium channels and is comprised of four subfamilies. Additionally we are shipping Potassium Voltage-Gated Channel, Shaw-Related Subfamily, Member 3 Antibodies (97) and many more products for this protein.
Showing 3 out of 7 products:
Kv3 (show KCNA3 Proteins) transcripts and proteins show a progressive increase in expression and reached an asymptote in adulthood, suggesting that the increase in Kv3 (show KCNA3 Proteins) expression during development might contribute to the maturation of the electrical activity of neurons.
Dendritic Kv3.3 potassium channels in mice cerebellar purkinje cells regulate generation and spatial dynamics of dendritic Ca2 (show CA2 Proteins)+ spikes.
Kv3.3 expression in Purkinje cells is necessary for normal motor speed but not gait pattern.
Motor deficits and altered synaptic transmission at the parallel fiber-Purkinje cell synapse in Kv3.3 knockout mice.
Double mutant Kv3.1 (show KCNC1 Proteins)/Kv3.3-deficient mice are constitutively hyperactive. Increased ambulatory and stereotypic activity in conjunction with sleep loss was seen in Kv3.1 (show KCNC1 Proteins)-single mutants but not in Kv3.3-single mutants.
two voltage-gated potassium channels, Kv3.1 (show KCNC1 Proteins) and Kv3.3, control sleep in wild-type and Kv3 (show KCNA3 Proteins)-mutant mice
We conclude that the rate of spontaneous action potential firing of Purkinje neurons is controlled by the interaction of Kv3.3 potassium currents and resurgent sodium currents.
In this study, we identified additional populations and subcellular compartments that are likely to sustain high-frequency firing because of the expression of Kv3.3 and other Kv3 (show KCNA3 Proteins) subunits.
Kv3.3 channels are required for generation of the repetitive spikelets of the complex spike.
Purkinje-cell-restricted restoration of Kv3.3 function restores complex spikes and rescues motor coordination in Kcnc3 mutants.
results therefore confirm the KCNC3R423H allele as causative for SCA13, through a dominant negative effect on KCNC3WT and links with EGFR (show EGFR Proteins) that account for dominant inheritance, congenital onset, and disease pathology
This review covers the localization and physiological function of Kv3.3 in the central nervous system and how the normal function of the channel is altered by the disease-causing mutations
Kv3.3 regulates Arp2/3-dependent cortical actin nucleation mediated by Hax-1; resulting cortical actin structures interact with the channel's gating machinery to slow its inactivation rate during sustained membrane depolarizations; a mutation that leads to late-onset spinocerebellar ataxia type 13.
The Kv channels, or at least Kv3.3, appear to be associated with cell differentiation
Functional and in silico analysis identified at least one novel pathogenic mutation in KCNC3 that cause Spinocerebellar ataxia type 13 (SCA13) and two additionally potential ones.
investigated using either targeted next generation sequencing or trio-based exome sequencing and were found to have mutations in three different genes, KCNC3, ITPR1 and SPTBN2
These results are specific to the KCNC3(R420H) allele and provide new insight into the molecular basis of disease manifestation in SCA13.
Data indicate that an autosomal dominant mutation in the gene encoding Kv3.3 has been identified in a large Filipino kindred manifesting as spinocerebellar ataxia type 13 (SCA13).
no disease-related KCNC3 mutation was identified, suggesting that spinocerebellar ataxia type 13 is a rare form of SCA in mainland China
Data suggest that mutant forms of Kv3.3 (as seem in subjects with spinocerebellar ataxia-13) are unstable, are degraded through proteasomes at faster rates, and can be stabilized by a chemical chaperone.
The Shaker gene family of Drosophila encodes components of voltage-gated potassium channels and is comprised of four subfamilies. Based on sequence similarity, this gene is similar to one of these subfamilies, namely the Shaw subfamily. The protein encoded by this gene belongs to the delayed rectifier class of channel proteins and is an integral membrane protein that mediates the voltage-dependent potassium ion permeability of excitable membranes.
potassium voltage-gated channel, Shaw-related subfamily, member 3
, potassium voltage-gated channel subfamily C member 3-like
, potassium voltage-gated channel subfamily C member 3
, voltage-gated potassium channel subunit Kv3.3
, Shaw-related voltage-gated potassium channel protein 3
, voltage-gated potassium channel protein KV3.3
, Shaw-related voltage-gated potassium channel protein 1
, potassium voltage gated channel, Shaw-related subfamily, member 1
, Shaw type potassium channel Kv3.3