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The results of this study shown the disruption of KV2.1 somato (show SSTR5 Proteins)-dendritic clusters prevents the apoptogenic increase of potassium currents.
KCNB1 oxidation may favor integrin clustering, thereby facilitating the recruitment and activation of FAK (show PTK2 Proteins) and Src (show SRC Proteins)/Fyn (show FYN Proteins) 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 (show KCNC4 Proteins) 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 Proteins)
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 Proteins) Ca2 (show CA2 Proteins)+ release channels
study supports the concept that transcriptional suppression of KV2.1 by activation of the AKAP150 (show AKAP5 Proteins)-CaN/NFATc3 (show NFATC3 Proteins) 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 Proteins)-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 Proteins)/JNK (show MAPK8 Proteins) signaling pathway.
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 Proteins) plays key role in mediating effect of leptin (show LEP Proteins) to modulate function of insulin (show INS Proteins)-secreting cells by promoting AMPK (show PRKAA1 Proteins)-dependent trafficking of KATP and Kv2.1 channels to plasma membrane. (NMDAR (show GRIN1 Proteins) = N-methyl-D-aspartate receptor (show GRIN1 Proteins); AMPK (show PRKAA1 Proteins) = AMP-activated protein kinase (show PRKAA2 Proteins); KATP = ATP-sensitive potassium channel (show KCNAB2 Proteins); Kv2.1 = delayed-rectifier potassium channel 1)
Kv2.1, but not Kv2.2 (KCNB2 (show KCNB2 Proteins)), forms clusters of 6-12 tetrameric channels at the plasma membrane and facilitates insulin (show INS Proteins) 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 Proteins)-3, Lys (show LYZ Proteins)-4, and Leu-5 (show TRIM13 Proteins) 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 Proteins)) 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 Proteins)+)/calmodulin does not interfere with the beta subunit's enzymatic activity as an NADPH (show NQO1 Proteins)-dependent oxidoreductase (show TXNRD1 Proteins), 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 Proteins) 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