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KCNA1 encodes a voltage-gated delayed potassium channel that is phylogenetically related to the Drosophila Shaker channel. Additionally we are shipping KCNA1 Proteins (7) and many more products for this protein.
Showing 10 out of 104 products:
Dog (Canine) Polyclonal KCNA1 Primary Antibody for WB - ABIN2776084
Tan, Lennon, Klein, Boeve, Pittock: Clinical spectrum of voltage-gated potassium channel autoimmunity. in Neurology 2008
Human Polyclonal KCNA1 Primary Antibody for IHC (p), WB - ABIN658604
Kim, Niethammer, Rothschild, Jan, Sheng: Clustering of Shaker-type K+ channels by interaction with a family of membrane-associated guanylate kinases. in Nature 1995
Human Polyclonal KCNA1 Primary Antibody for WB - ABIN265021
Baumann, Grupe, Ackermann, Pongs: Structure of the voltage-dependent potassium channel is highly conserved from Drosophila to vertebrate central nervous systems. in The EMBO journal 1989
Human Polyclonal KCNA1 Primary Antibody for EIA, IHC (p) - ABIN952993
Graves, Rajakulendran, Zuberi, Morris, Schorge, Hanna, Kullmann: Nongenetic factors influence severity of episodic ataxia type 1 in monozygotic twins. in Neurology 2010
This study provide new insights into the dynamic and differential distribution of Kv1 (show KCNA5 Antibodies) channels and associated proteins during myelination.
age-associated changes in Sphingolipid composition or CerS2 (show CERS2 Antibodies) ablation upregulate K(Ca) 1.1 and impair Ca(2 (show CA2 Antibodies)+) mobilization, which thereby induces contractile dysfunction of gastric smooth muscle.
Kcna-1 null mice initially expressed only a few of the most severe seizure types that progressively increased in frequency and decreased in seizure severity
Kv1.2 (show KCNA2 Antibodies) channels represent an important physiological link in electric field-induced cell migration.
Spontaneous seizures in Kcna1-null mice activate Fos expression in select limbic circuits
Data suggest that the behavioral effect of Kv1.1 (show KCNA2 Antibodies) deletion is primarily to impede binaural integration and thus to mimic monaural hearing.
The Kv1.1 (show KCNA2 Antibodies) null mouse is a potential model for sudden unexpected death in epilepsy in patients
Kv1.1 (show KCNA2 Antibodies) is modulated by ANK3 (show ANK3 Antibodies) in conditions of high dietary magnesium
these data indicate that loss of Kv1.1 (show KCNA2 Antibodies) enhances synaptic release in the CA3 (show CA3 Antibodies) region, which reduces spike timing precision of individual neurons leading to disorganization of network oscillatory activity and promotes the emergence of fast ripples.
Kv1.1 (show KCNA2 Antibodies) acts as a mechanosensitive brake that regulates mechanical sensitivity of fibers associated with mechanical perception
we demonstrate that the pathophysiological impact of the I262T mutation entails altered channel gating and defective protein biosynthesis, both of which raise imperative questions that call for further elucidation of the structural and functional roles of the S3 transmembrane segment in Kv1.1 channels.
Herein, we critically evaluate the molecular and biophysical characteristics of the KV1.1 protein in comparison with others and discuss their role in the greater penetrance of KCNA1 mutations in humans leading to the neurological signs of episodic ataxia (show USP14 Antibodies) type 1
KCNA1 mutations should be considered in patients of all ages with episodic neurological phenotypes, even when ataxia (show USP14 Antibodies) is not present.
These findings provide evidence of an intrinsic cardiac role of Kv1.1 channels and indicate that they may contribute to atrial repolarization and atrial fibrillation susceptibility.
Fine-tuning of Kv1.1 surface expression by RNA editing might contribute to the complexity of neuronal Kv channel regulation.
Novel mutations in KCNA1 genes are associated with episodic ataxia (show USP14 Antibodies) type 1.
Using mutagenesis and analysis of gating currents from gating pore mutations in the Shaker Kv channel, we identified statistically highly significant correlations between VSD function and physicochemical properties of gating pore residues.
The combination of copy number variant and SNPs in KCNA1 (and SCN1A (show SCN1A Antibodies)) genes increased the risk for both epilepsy and premature death.
New mutations (R167M, C185W and I407M) were identified in three out of the four families. When expressed in human embryonic kidney cells, all three new mutations resulted in a loss of K(v)1.1 (show KCNA2 Antibodies) channel function.
characterization of mutations in the potassium channel (show KCNAB2 Antibodies) Kv1.1
This gene encodes a voltage-gated delayed potassium channel that is phylogenetically related to the Drosophila Shaker channel. The encoded protein has six putative transmembrane segments (S1-S6), and the loop between S5 and S6 forms the pore and contains the conserved selectivity filter motif (GYGD). The functional channel is a homotetramer. The N-terminus of the channel is associated with beta subunits that can modify the inactivation properties of the channel as well as affect expression levels. The C-terminus of the channel is complexed to a PDZ domain protein that is responsible for channel targeting. Mutations in this gene have been associated with myokymia with periodic ataxia (AEMK).
potassium voltage-gated channel, shaker-related subfamily, member 1 (episodic ataxia with myokymia)
, voltage-gated potassium channel Kv1.1
, potassium voltage-gated channel, shaker-related subfamily, member 1
, voltage-gated potassium channel
, potassium voltage-gated channel subfamily A member 1
, potassium voltage-gated channel subfamily A member 1-like
, brain potassium channel protein-1
, potassium voltage gated channel, shaker related subfamily, member 1
, voltage-gated potassium channel subunit Kv1.1
, potassium (K+) channel protein voltage dependent
, potassium voltage gated channel shaker related subfamily member 1
, voltage-gated K(+) channel HuKI
, voltage-gated potassium channel HBK1