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Ca(v)2.3 Ca2+ channel interacts with the G1-subunit of V-ATPase.
The present molecular characterization of the Ca(v)2.2 channel provides novel biochemical evidence for an N-type channel in hair cells, and details molecular interactions of this channel that reflect hair-cell function.
This study identified a polymorphism in exon 20 of the CACNA1E gene (Asp859Glu - rs35737760) that is more prevalent in hemiplegic and brain stem aura migraine.
Carriers of the minor G allele of the rs3845446 SNP exhibited enhanced pain-related phenotypes after gastrointestinal surgery. The pain-related phenotypes of carriers of the minor allele of this SNP after gastrointestinal surgery were opposite to such phenotypes after orthognathic surgery.
Data suggest that, in vascular smooth muscle cells, increase in cytosolic endothelin-1 (EDN1) induces sustained increase in nuclear Ca2+ via stimulation of R-type calcium channel (CACNA1E) present at the nuclear membrane.
CACNA1E gene single nucleotide polymorphisms may be involved in fentanyl sensitivity.
The C-terminus of human Ca(v)2.3 voltage-gated calcium channel interacts with alternatively spliced calmodulin-2 expressed in two human cell lines
quartet of leucine residues in the guanylate kinase domain of CaVbeta determines the plasma membrane density of the CaV2.3 channel.
CACNA1E variants affect beta cell function in patients with newly diagnosed type 2 diabetes.
the II-III loop of the Ca(v)2.3 calcium channel binds APLP1 and that this binding promotes internalization of the channel
Lack of high-voltage activated Cav2.3 channels results in a marked decrease in the sensitivity of transgenic animals to gamma-butyrolactone-induced absence epilepsy.
Swapping the I-II intracellular linker between L-type CaV1.2 and R-type CaV2.3 high-voltage gated calcium channels exchanges activation attributes.
Review discusses the roles of Cav2.3-containing E-type Ca2+ channels which exhibit several subunit-specific features, trigger exocytosis and are also involved in long-term potentiation.
Full-length RGS3, RGS3T, and the core domain of RGS3 were equally effective in antagonizing inhibition of Ca(V)2.3 through M(2)R.
Neurokinin 1 receptorsmodulate CaV2.3 using three different signaling mechanisms: a fast inhibition mediated by Gbeta gamma, a slow inhibition mediated by Galpha(q/11), and a slow stimulation mediated by protein kinases C.
Amplification and overexpression of CACNA1E correlates with relapse in favorable histology Wilms' tumors.
analysis of a three-dimensional homology model of Ca(V)2.3 based upon Kv1.2 where hydrophobic residues at positions facing Val(1720) in IS6, IIS6, and IIIS6 play a critical role in stabilizing the closed state in Ca(V)2.3
A functional variant in CACNA1E contributes to type 2 diabetes susceptibility in Pima indians by affecting insulin action.
Genetic variation in the CACNA1E gene contributes to an increased risk of the development of type 2 diabetes by reducing insulin secretion.
These findings strongly suggest that both H179 and H183 in the IS3-IS4 loop are essential structural determinants required for nickel sensitive inhibition of the Cav2.3.
The ex vivo neuronal setup of the isolated and superfused murine retina demonstrates a transient effect of bilirubin on neuronal signaling only when Cav2.3/R-type channels are present. Modulation of Cav2.3/R-type Ca2+ channels may contribute to the pathophysiological cascades of vasospasm or delayed cerebral ischemia.
The results of this study showed that Cav2.3 is a novel mechanistic target for a key pronociceptive miRNA, miR-34c-5p.
Data show that apamin boosts evoked excitatory postsynaptic potentials (EPSPs) in CaV2.3 R-Type Ca2+ Channel knockout (CaV2.3-/-) mice.
under conditions of Zn2+ deficiency, ablation or dysfunction of Cav2.3 channels may lead to severe disturbances in glucose homeostasis.
Cav2.1-2.3 have unique contributions to the dynamics at the Schaffer collateral synapse that are engaged by the complex patterns of afferent activity seen in vivo
Low-voltage activated CaV2.3 R-type Ca(2+) channels in the thalamocortical loop and extra-thalamocortical circuitries substantially regulate rodent sleep architecture and represent a novel potential target for pharmacological treatment of sleep disorders
Cacna1e expression (and Cacna1h) is essential for paraventricular hypothalamic neuronal activity and preventing hyperphagia.
Cav2.3 does not only contribute to the cardiac autonomous nervous system but also to intrinsic rhythm propagation.
This study demonistrated that Immunogold particles were observed over the plasma membrane of dendritic spines of neurin in brain, including both synaptic and extrasynaptic sites
Cav2.3 voltage-gated divalent calcium channels (VGCC) are an important factor in septohippocampal synchronization associated with theta; oscillation.
stimulation with exogenous PACAP and native neuronal stress stimulation both lead to a PKC-mediated phosphodependent recruitment of a T-type Ca(v)3.2 Ca(2+) influx, which in turn evokes catecholamine release during the acute sympathetic stress response
Both high-affinity Ni(2+)-sensitive Ca(2+) channels contribute to transretinal signalling.
role in calcium currents in spermatocytes
functional role for the Ca(v)2.3 subunit in hormone secretion and glucose homeostasis
Ca(v)2.3 (alpha1E) Ca2+ channel participates in the control of sperm function.
the postsynaptic role of the R-type channel in the propagation of excitation and other mechanisms underlying the increased halothane MAC(RR) in Ca(v)2.3(-/-) mice
The presence of Cav2.3 channels boosts accumulation of presynaptic Ca2+ triggering presynaptic LTP and posttetanic potentiation without affecting low release probability required for the enormous plasticity displayed by mossy fiber synapses.
Cav2.3 immunoreactivity was found in the outer spiral bundle followed by the inner spiral bundle, efferent endings and by medial efferent fibers
a specific role for Ca(V)2.3 Ca(2+) channels in second-phase insulin release, that of mediating the Ca(2+) entry needed for replenishment of the releasable pool of granules as well as islet cell differentiation
Data suggest that Ca(v)2.3 containing R-type voltage-gated Ca2+ channels are involved in the glucose-mediated signalling to glucagon release.
Inhibition of CaV2.3 channels by NK1 receptors is sensitive to membrane cholesterol but insensitive to caveolin-1.
Voltage-dependent calcium channels are multisubunit complexes consisting of alpha-1, alpha-2, beta, and delta subunits in a 1:1:1:1 ratio. These channels mediate the entry of calcium ions into excitable cells, and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. This gene encodes the alpha-1E subunit of the R-type calcium channels, which belong to the 'high-voltage activated' group that maybe involved in the modulation of firing patterns of neurons important for information processing. Alternatively spliced transcript variants encoding different isoforms have been described for this gene.
voltage-dependent R-type calcium channel subunit alpha-1E
, voltage-gated calcium channel alpha 1E subunit
, calcium channel, voltage-dependent, R type, alpha 1E subunit
, brain calcium channel II
, calcium channel, L type, alpha-1 polypeptide
, calcium channel, R type, alpha-1 polypeptide
, calcium channel, voltage-dependent, alpha 1E subunit
, voltage-dependent calcium channel alpha 1E subunit
, voltage-gated calcium channel alpha subunit Cav2.3
, voltage-gated calcium channel subunit alpha Cav2.3
, calcium channel, voltage-dependent, L type, alpha 1E subunit
, voltage gated calcium channel alpha1E subunit
, voltage-dependent calcium channel alpha1-E subunit
, brain calcium channel BII-1
, brain calcium channel BII-2