Calcium Channel, Voltage-Dependent, N Type, alpha 1B Subunit (CACNA1B) ELISA Kits

Human Calcium Channel, Voltage-Dependent, N Type, alpha 1B Subunit (CACNA1B) interaction partners

1. 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.

2. 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.

3. These results do not support a causal association between the CACNA1B c.4166G>A; (p.R1389H) variant and M-D.

4. the consensus motifs of S-nitrosylation were much more abundant in Cav2.2 than in Cav1.2 and Cav2.1.

5. AP-1 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

6. CACNA1B mutation is linked to unique myoclonus-dystonia syndrome.

7. The first disease connection for Cav2.2 channels [review]

8. The interaction between LC1 and the N-type channel (CaV2.2 channel) was demonstrated.

9. 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

10. Results show that GABA(B) receptors R1 and R2 must be activated for the modulation of N-type (Ca(v)2.2) calcium channels by analgesic alpha-conotoxins Vc1.1 and RgIA.

11. new mechanistic perspectives, and reveal unexpected variations in determinants, underlying inhibition of Ca(V)1.2/Ca(V)2.2 channels by distinct RGK GTPases.

12. Ca(2+) exits the channel through the Cav2.2.

13. polymorphisms and haplotypes in the human CACNA1B gene show significant differences between cerebral infarction and control patients

14. Results suggest that a 39 bp DNA element in the N-type voltage-gated calcium channel alpha1B gene might act as repressor in non-neuronal cells through specific interactions with DNA.

15. molecular dissection of calcium current mechanosensitivity- electrophysiology of N-type calcium channels

16. the C-terminal region of Ca(v)2.2 does not have a critical role in regulation of the calcium channel

17. Cav2.2 alpha2delta auxiliary subunit binds to omega-conotoxins

18. Activation of PKC resulted in its recruitment to and phosphorylation of Ca(V)2.2 channels, but PKC phosphorylation did not dissociate Ca(V)2.2 channel/syntaxin 1A complexes.

19. The Y388S mutation had no effect on current density and cell surface expression of Ca(V)2.2/alpha2delta-2/beta1b channels expressed in human embryonic kidney tsA-201 cells, when equivalent proportions of cDNA were used.

20. Our studies of the e37a/e37b splice site reveal a multifunctional domain in the C-terminus of Ca(V)2.2 that regulates the overall activity of N-type calcium channels in nociceptors.

Mouse (Murine) Calcium Channel, Voltage-Dependent, N Type, alpha 1B Subunit (CACNA1B) interaction partners

1. Munc13-3 regulates the density of Cav2.1 and Cav2.2 channels, alters the localization of Cav2.1, and is required for the development of tight, nanodomain coupling at parallel-fiber active zones.

2. It is essential for presynaptic neurotransmitter release.

3. Thus, GHSR1a differentially inhibits CaV2 channels by Gi/o or Gq protein pathways depending on its mode of activation.

4. Blockade of Cav2.2 in inflammatory arthritis leads to up-regulation of the osteoclast activator RANKL and concomitant joint and bone destruction.

5. 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

6. Both pharmacological blockade of N-type calcium channels and their genetic titration improved cardiac autonomic balance and prevented lethal arrhythmias in a mouse model of dilated cardiomyopathy and sudden arrhythmic death.

7. Gaba B receptors were found to mediate Cav2.2 channel inhibition.

8. 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

9. Results demonstrate that sensory neurons from Nf1+/- mice, exhibit increased N-type (Cav2.2) ICa and likely account for the increased release of substance P and calcitonin gene-related peptide that occurs in Nf1+/- sensory neurons

10. data suggest that the different roles that Ca(V)2.1 and Ca(V)2.2 play in MNC secretion may be a result of the different levels of expression of Ca(V)2.1 in VP and OT MNCs

11. Although the mechanism of its activation is not clear at present, activation of N-type VDCC expressed in non-excitable microglial cells contributes to the pathophysiology of neuropathic pain.

12. CaV2.2 and alpha2delta-1 are intimately associated at the plasma membrane

13. These findings identify an interaction between ankyrin-B and both Cav2.1 and Cav2.2 at the amino acid level that is necessary for proper Cav2.1 and Cav2.2 targeting in vivo.

14. Oxidative stress-related endothelial dysfunction induced by angiotensin II is suppressed in mice lacking the N-type VDCC alpha1B subunit.

15. Blocking Cav2.2 channels abolishes respiratory activity in all brainstem slices from Cav2.1 genetically ablated animals.

16. High focal axoplasmic Ca2+ levels correlate with focal aggregation of the reverse Na+/Ca2+ exchanger 1, voltage-gated N-type Ca2+ channel alpha1B subunit, and actin at the sites of spheroids in individual axons.

17. This study demonistrated that Cacna1b gene expression in mouse dorsal raphe nucleus

18. Presynaptic VDCCs link the target-derived synapse organizer laminin beta2 to active-zone proteins and function as scaffolding proteins to anchor active-zone proteins to the presynaptic membrane.

19. this study suggested that highly specialized, discrete cellular responsiveness in vivo can be attributed to alternative splicing events regulated at the level of individual neurons.

20. These results suggest that Ca(2+) in the central nervous system modulates various neurophysiological functions, such as locomotor activity, long-term memory, and sensorimotor gating through the alpha(1B) subunit of the N-type calcium channels.

Rabbit Calcium Channel, Voltage-Dependent, N Type, alpha 1B Subunit (CACNA1B) interaction partners

1. Structural flexibility of CaV1.2 and CaV2.2 I-II proximal linker

2. these results unveil a novel functional coupling between Parkin and the CaV2.2 channels

3. The CaVbeta Subunit Protects the I-II Loop of the Voltage-gated Calcium Channel CaV2.2 from Proteasomal Degradation but Not Oligoubiquitination.

4. The monomeric G proteins AGS1 and Rhes selectively influence Galphai-dependent signaling to modulate N-type (CaV2.2) calcium channels.