Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
The protein encoded by CACNA1B is the pore-forming subunit of an N-type voltage-dependent calcium channel, which controls neurotransmitter release from neurons. Additionally we are shipping CACNA1B Kits (12) and CACNA1B Proteins (9) and many more products for this protein.
Showing 10 out of 55 products:
Rat (Rattus) Polyclonal CACNA1B Primary Antibody for 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. in Nature communications 2015
Cav2.2 alpha1 subunit alone could form a complex with the AMPAR in heterologous cells. The cell-surface AMPAR was increased by co-expression of Cav2.2 alpha1 subunit.
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 (show CACNA1C Antibodies) and Cav2.1 (show CACNA1A Antibodies).
AP-1 (show FOSB Antibodies) 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 (show MAP1B Antibodies) 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 (show CACNA1C Antibodies)/Ca(V)2.2 channels by distinct RGK GTPases.
Thus, GHSR1a differentially inhibits CaV2 (show CAV2 Antibodies) 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 (show TNFSF11 Antibodies) 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 (show CACNA1A Antibodies)-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 (show NF1 Antibodies)+/- mice, exhibit increased N-type (Cav2.2) ICa and likely account for the increased release of substance P (show TAC1 Antibodies) and calcitonin gene-related peptide (show CALCA Antibodies) that occurs in Nf1 (show NF1 Antibodies)+/- sensory neurons
data suggest that the different roles that Ca(V)2.1 (show CACNA1A Antibodies) and Ca(V)2.2 play in MNC secretion may be a result of the different levels of expression of Ca(V)2.1 (show CACNA1A Antibodies) 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 (show ANK2 Antibodies) and both Cav2.1 (show CACNA1A Antibodies) and Cav2.2 at the amino acid level that is necessary for proper Cav2.1 (show CACNA1A Antibodies) and Cav2.2 targeting in vivo.
Blocking Cav2.2 channels abolishes respiratory activity in all brainstem slices from Cav2.1 (show CACNA1A Antibodies) genetically ablated animals.
Structural flexibility of CaV1.2 (show CACNA1C Antibodies) and CaV2.2 I-II proximal linker
these results unveil a novel functional coupling between Parkin (show PARK2 Antibodies) 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 (show RASD1 Antibodies) and Rhes (show RASD2 Antibodies) 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