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