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Mammalian Monoclonal KCNB1 Primary Antibody for ISt, IHC - ABIN1304758
Krasowska, Zabłocki, Górecki, Swinny: Aberrant location of inhibitory synaptic marker proteins in the hippocampus of dystrophin-deficient mice: implications for cognitive impairment in duchenne muscular dystrophy. in PLoS ONE 2014
Show all 74 Pubmed References
Mammalian Monoclonal KCNB1 Primary Antibody for ISt, IHC - ABIN1304759
Mohapatra, Siino, Trimmer: Interdomain cytoplasmic interactions govern the intracellular trafficking, gating, and modulation of the Kv2.1 channel. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2008
Show all 13 Pubmed References
Cow (Bovine) Polyclonal KCNB1 Primary Antibody for ELISA - ABIN548205
Park, Mohapatra, Misonou, Trimmer: Graded regulation of the Kv2.1 potassium channel by variable phosphorylation. in Science (New York, N.Y.) 2006
Kv8.2 knock-out (KO) mice show many similarities to human cone dystrophy with a supernormal rod response, including a depressed a-wave and an elevated b-wave response with bright light stimulation. Optical coherence tomography imaging and immunohistochemistry indicate that the changes in six-month-old Kv8.2 KO retinae are largely limited to the outer nuclear layer, while outer segments appear intact.
these findings demonstrate a conserved in vivo function for Kv2 family members in remodeling neuronal endoplasmic reticulum-plasma membrane junctions.
The results of this study shown the disruption of KV2.1 somato-dendritic clusters prevents the apoptogenic increase of potassium currents.
KCNB1 oxidation may favor integrin clustering, thereby facilitating the recruitment and activation of FAK and Src/Fyn kinases.
Spinal Musculature Atrophy motor neurons showed a lower surface expression of Kv2.1 potassium channels and reduced spiking ability.
This study provides the first experimental evidence that oxidation of a K(+) channel constitutes a mechanism of neuronal and cognitive impairment in vertebrates. Specifically, the interaction of KCNB1 channels with reactive oxygen species plays a major role in the etiology of mouse model of traumatic brain injury (TBI), a condition associated with extensive oxidative stress. In addition, a Food and Drug Administration-app
The AMIGO1-KCNB1 complex is involved in schizophrenia-related behavioral domains in mice.
major finding from this study is the novel region- and cell-specific relationship between the localization of the plasma membrane Kv2.1 channel and intracellular RyR Ca2+ release channels
study supports the concept that transcriptional suppression of KV2.1 by activation of the AKAP150-CaN/NFATc3 signaling axis contributes to enhanced arterial tone during diabetes
High temperature sensitivity is intrinsic to voltage-gated potassium channels.
These results showed that a modest suppression of Kv2.1 channels dramatically raises insulinotropic potency of GLP-1-based drugs.
Kv2.1 knockout mice are strikingly hyperactive, defective in spatial learning and hypersensitive to convulsants.
the accumulation of KCNB1 oligomers in the membrane disrupts planar lipid raft integrity and causes apoptosis via activating the c-Src/JNK signaling pathway.
Kv2.1 regulates insulin secretion in beta-cells
Direct interaction between syntaxin 1A and the Kv2.1 C-terminus is required for efficient insulin exocytosis and glucose-stimulated insulin secretion.
stromatoxin-1 -sensitive KV2-containing channels are expressed in detrusor smooth muscle (DSM); they control DSM excitability, intracellular Ca2+ levels, and myogenic and nerve-evoked contractions
Hypoxic preconditioning enhances the ability of mesenchymal stem cell migration; this effect is mediated through a regulatory role of Kv2.1 on FAK phosphorylation/activation.
These results suggest that Kv2.1 is tightly regulated in a clinically relevant animal model of anoxia and further implicate its role in the homeostasis of neurons during anoxic stress.
Prolonged high glucose exposure increases both Kv current amplitude and the primary Kv channel subunit (Kv2.1) expression in mouse pancreatic beta-cells and reduces angiotensin II type 2 receptor expression.
data indicate that the spatially restrictive upregulation of Kv2.1-encoded currents underlies the increased dispersion of the repolarization observed in Kv1DN mice.
Both factors could be regulating the Kv2.1 channel.
KCNB1 is a novel prognostic factor for gliomas that exerts its tumor suppressive function through autophagy induction.
PIP2 regulates Kv2.1 channels by interfering with the inactivation mechanism.
The results of this study support the conclusion that the KCNB1 variants described here are likely to be pathogenic in patient with Neurodevelopmental Disorders.
Data suggest that NMDAR plays key role in mediating effect of leptin to modulate function of insulin-secreting cells by promoting AMPK-dependent trafficking of KATP and Kv2.1 channels to plasma membrane. (NMDAR = N-methyl-D-aspartate receptor; AMPK = AMP-activated protein kinase; KATP = ATP-sensitive potassium channel; Kv2.1 = delayed-rectifier potassium channel 1)
Kv2.1, but not Kv2.2 (KCNB2), forms clusters of 6-12 tetrameric channels at the plasma membrane and facilitates insulin exocytosis. Knockdown of Kv2.1 expression reduces secretory granule targeting to the plasma membrane. KCNB1 appears reduced in T2D islets, and further knockdown of KCNB1 does not inhibit Kv current in T2D beta-cells. Upregulation of Kv2.1-wild-type, but not Kv2.1-DeltaC318, rescues the exocytotic phen...
the first six N-terminal residues including Lys-3, Lys-4, and Leu-5 are critical for controlling functional regulation, but not trafficking, of BK channels. This membrane-distal region has features of an amphipathic helix that is predicted to control the orientation of the first transmembrane-spanning domain (TM1) of the beta1-subunit.
Perifosine modified the Kv2.1 inactivation gating resulting in a decrease of the current amplitude.
KCNB1 is a strong susceptibility gene for schizophrenia spectrum disorders in humans.
inactivation regulation via Ca(2+)/calmodulin does not interfere with the beta subunit's enzymatic activity as an NADPH-dependent oxidoreductase, thus rendering the Kvb1.1 subunit a multifunctional receptor
Kv2.1 functional aberrations in humans are associated with developmental delay, infantile generalized seizures, hypotonia, and behavioural problems, and also highlight a critical role for Kv2.1 in regulating neuronal firing in neuronal circuits.
Epileptic V378A variant in KCNB1 changes ion selectivity, trafficking and expression of Kv2.1 channel.
KCNE5 subunits may affect Kv2.1 homotetramers and Kv2.1/Kv6.4 heterotetramers in vivo, resulting in more tissue-specific fine-tuning mechanisms.
KvS subunits modify the pharmacological response of Kv2 subunits when assembled in heterotetramers and illustrate the potential of KvS subunits to provide unique properties to the heterotetramers, as is the case for 4-AP on Kv2.1/Kv6.4 channels.
The results indicate that KCNB1 is likely associated with metabolic traits that may either predispose or protect from progression to metabolic syndrome.
Glutamate exposure results in a loss of Kv2.1 clusters in neurons.
HO-1 expression can strongly influence apoptosis via CO-mediated regulation of Kv2.1 activity
This study identified a de novo missense mutation in KCNB1 that encodes the KV 2.1 voltage-gated potassium channel.
In cerebellar granule cells, regulation of Kv2.1 by GDF15 is mediated through the TGFbetaRII-activated Akt/mTOR pathway.
The KCNB1 rs1051295 TT genotype is associated with decreased insulin sensitivity.
Analysis of the data suggested that Kv2.1 channels contribute significantly to the voltage-gated potassium current in smooth muscle cells from rabbit urethra.
Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shab-related subfamily. This member is a delayed rectifier potassium channel and its activity is modulated by some other family members.
Voltage-gated potassium channel subunit Kv2.1
, potassium voltage-gated channel subfamily B member 1
, potassium voltage-gated channel, Shab-related subfamily, member 1
, voltage gated potassium channel subtype 2.1
, potassium voltage-gated channel subfamily B member 1-like
, delayed rectifier potassium channel 1
, voltage-gated potassium channel subunit Kv2.1
, potassium channel Kv2.1
, delayed rectifier potassium channel Kv2.1
, h-DRK1 K(+) channel
, potassium channel protein DRK1
, voltage-gated potassium channel Kv2.1