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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. Additionally we are shipping CACNA1B Kits (8) and CACNA1B Proteins (6) and many more products for this protein.
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Human Polyclonal CACNA1B Primary Antibody for IHC, WB - ABIN350135
Humphray, Oliver, Hunt, Plumb, Loveland, Howe, Andrews, Searle, Hunt, Scott, Jones, Ainscough, Almeida, Ambrose, Ashwell, Babbage, Babbage, Bagguley, Bailey, Banerjee, Barker, Barlow, Bates, Beasley et al.: DNA sequence and analysis of human chromosome 9. ... in Nature 2004
Show all 4 references for ABIN350135
Human Polyclonal CACNA1B Primary Antibody for IHC - ABIN965734
Coppola, Waldmann, Borsotto, Heurteaux, Romey, Mattéi, Lazdunski: Molecular cloning of a murine N-type calcium channel alpha 1 subunit. Evidence for isoforms, brain distribution, and chromosomal localization. in FEBS letters 1994
Show all 2 references for ABIN965734
Human Polyclonal CACNA1B Primary Antibody for ICC, IHC - ABIN1742169
Scheuber, Miles, Poncer: Presynaptic Cav2.1 and Cav2.2 differentially influence release dynamics at hippocampal excitatory synapses. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2004
Human Polyclonal CACNA1B Primary Antibody for WB - ABIN265031
Dubel, Starr, Hell, Ahlijanian, Enyeart, Catterall, Snutch: Molecular cloning of the alpha-1 subunit of an omega-conotoxin-sensitive calcium channel. in Proceedings of the National Academy of Sciences of the United States of America 1992
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.
Ca(2 (show CA2 Antibodies)+) exits the channel through the Cav2.2.
polymorphisms and haplotypes in the human CACNA1B gene show significant differences between cerebral infarction and control patients
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.
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