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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
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 (show KCNC4 Antibodies) 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 (show APP Antibodies)
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 (show RYR1 Antibodies) Ca2 (show CA2 Antibodies)+ release channels
study supports the concept that transcriptional suppression of KV2.1 by activation of the AKAP150 (show AKAP5 Antibodies)-CaN/NFATc3 (show NFATC3 Antibodies) signaling axis contributes to enhanced arterial tone during diabetes
These results showed that a modest suppression of Kv2.1 channels dramatically raises insulinotropic potency of GLP-1 (show GCG Antibodies)-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 (show SRC Antibodies)/JNK (show MAPK8 Antibodies) signaling pathway.
Kv2.1 regulates insulin (show INS Antibodies) secretion in beta-cells
Direct interaction between syntaxin 1A (show STX1A Antibodies) and the Kv2.1 C-terminus is required for efficient insulin (show INS Antibodies) exocytosis and glucose-stimulated insulin (show INS Antibodies) secretion.
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 (show GRIN1 Antibodies) plays key role in mediating effect of leptin (show LEP Antibodies) to modulate function of insulin (show INS Antibodies)-secreting cells by promoting AMPK (show PRKAA1 Antibodies)-dependent trafficking of KATP and Kv2.1 channels to plasma membrane. (NMDAR (show GRIN1 Antibodies) = N-methyl-D-aspartate receptor (show GRIN1 Antibodies); AMPK (show PRKAA1 Antibodies) = AMP-activated protein kinase (show PRKAA2 Antibodies); KATP = ATP-sensitive potassium channel (show KCNAB2 Antibodies); Kv2.1 = delayed-rectifier potassium channel 1)
Kv2.1, but not Kv2.2 (KCNB2 (show KCNB2 Antibodies)), forms clusters of 6-12 tetrameric channels at the plasma membrane and facilitates insulin (show INS Antibodies) 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 (show LYZ Antibodies)-3, Lys (show LYZ Antibodies)-4, and Leu-5 (show TRIM13 Antibodies) 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 (show TPM2 Antibodies)) 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 (show CA2 Antibodies)+)/calmodulin (show CALM1 Antibodies) does not interfere with the beta subunit's enzymatic activity as an NADPH (show NQO1 Antibodies)-dependent oxidoreductase (show TXNRD1 Antibodies), 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 (show Kcng4 Antibodies) heterotetramers in vivo, resulting in more tissue-specific fine-tuning mechanisms.
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