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The protein encoded by CACNA1B is the pore-forming subunit of an N-type voltage-dependent calcium channel, which controls neurotransmitter release from neurons. De plus, nous expédions CACNA1B Kits (12) et CACNA1B Protéines (6) et beaucoup plus de produits pour cette protéine.
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Rat (Rattus) Polyclonal CACNA1B Primary Antibody pour WB - ABIN1742327
Lenkey, Kirizs, Holderith, Máté, Szabó, Vizi, Hájos, Nusser: Tonic endocannabinoid-mediated modulation of GABA release is independent of the CB1 content of axon terminals. dans Nature communications 2015
CACNA1B protein expressions in tumorous tissues were correlated with NSCLC patients' clinical characteristics and overall survival. CACNA1B mRNA and protein expression levels were higher in NSCLC tumorous tissues than in nontumorous tissues.
These results do not support a causal association between the CACNA1B c.4166G>A; (p.R1389H) variant and M-D.
the consensus motifs of S-nitrosylation were much more abundant in Cav2.2 than in Cav1.2 (Montrer CACNA1C Anticorps) and Cav2.1 (Montrer CACNA1A Anticorps).
AP-1 (Montrer FOSB Anticorps) binding motifs, present only in exon 37a, enhance intracellular trafficking of exon 37a-containing Ca(V)2.2 to the axons and plasma membrane of rat dorsal root ganglia neurons
CACNA1B mutation is linked to unique myoclonus-dystonia syndrome.
The first disease connection for Cav2.2 channels [review]
The interaction between LC1 (Montrer MAP1B Anticorps) and the N-type channel (CaV2.2 channel) was demonstrated.
with membrane-localized CaV beta subunits, CaV2.2 channels are subject to Gbetagamma-mediated voltage-dependent inhibition, whereas cytosol-localized beta subunits confer more effective PIP2-mediated voltage-independent regulation
new mechanistic perspectives, and reveal unexpected variations in determinants, underlying inhibition of Ca(V)1.2 (Montrer CACNA1C Anticorps)/Ca(V)2.2 channels by distinct RGK GTPases.
Ca(2 (Montrer CA2 Anticorps)+) exits the channel through the Cav2.2.
Thus, GHSR1a differentially inhibits CaV2 (Montrer CAV2 Anticorps) channels by Gi/o or Gq protein pathways depending on its mode of activation.
Blockade of Cav2.2 in inflammatory arthritis leads to up-regulation of the osteoclast activator RANKL (Montrer TNFSF11 Anticorps) and concomitant joint and bone destruction.
Results identified altered synaptic transmission in the olfactory system of Cav2.2-deficient mice and suggest that the olfactory system could become an attractive model to learn more about this channel and the consequences of its removal
Gaba B receptors were found to mediate Cav2.2 channel inhibition.
Cav2.1 (Montrer CACNA1A Anticorps)-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
Results demonstrate that sensory neurons from Nf1 (Montrer NF1 Anticorps)+/- mice, exhibit increased N-type (Cav2.2) ICa and likely account for the increased release of substance P (Montrer TAC1 Anticorps) and calcitonin gene-related peptide (Montrer CALCA Anticorps) that occurs in Nf1 (Montrer NF1 Anticorps)+/- sensory neurons
data suggest that the different roles that Ca(V)2.1 (Montrer CACNA1A Anticorps) and Ca(V)2.2 play in MNC secretion may be a result of the different levels of expression of Ca(V)2.1 (Montrer CACNA1A Anticorps) in VP and OT MNCs
CaV2.2 and alpha2delta-1 are intimately associated at the plasma membrane
These findings identify an interaction between ankyrin-B (Montrer ANK2 Anticorps) and both Cav2.1 (Montrer CACNA1A Anticorps) and Cav2.2 at the amino acid level that is necessary for proper Cav2.1 (Montrer CACNA1A Anticorps) and Cav2.2 targeting in vivo.
Blocking Cav2.2 channels abolishes respiratory activity in all brainstem slices from Cav2.1 (Montrer CACNA1A Anticorps) genetically ablated animals.
these results unveil a novel functional coupling between Parkin (Montrer PARK2 Anticorps) and the CaV2.2 channels
The CaVbeta Subunit Protects the I-II Loop of the Voltage-gated Calcium Channel CaV2.2 from Proteasomal Degradation but Not Oligoubiquitination.
The monomeric G proteins AGS1 (Montrer RASD1 Anticorps) and Rhes (Montrer RASD2 Anticorps) selectively influence Galphai-dependent signaling to modulate N-type (CaV2.2) calcium channels.
The protein encoded by this gene is the pore-forming subunit of an N-type voltage-dependent calcium channel, which controls neurotransmitter release from neurons. The encoded protein forms a complex with alpha-2, beta, and delta subunits to form the high-voltage activated channel. This channel is sensitive to omega-conotoxin-GVIA and omega-agatoxin-IIIA but insensitive to dihydropyridines. Two transcript variants encoding different isoforms have been found for this gene.
calcium channel, voltage-dependent, L type, alpha 1B subunit
, voltage-dependent N-type calcium channel subunit alpha-1B
, calcium channel, voltage-dependent, N type, alpha 1B subunit
, Cav2.2 voltage-gated Ca2+ channel
, brain calcium channel III
, calcium channel alpha12.2 subunit
, calcium channel, L type, alpha-1 polypeptide
, calcium channel, N type
, calcium channel, voltage-dependent, alpha 1B subunit, N type
, voltage-gated calcium channel alpha subunit Cav2.2
, voltage-gated calcium channel subunit alpha Cav2.2
, voltage gated N-type calcium channel Ca(v)2.2
, N-type voltage-gated calcium channel alpha1B subunit ChCaChA1B
, calcium channel BIII