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anti-Human CACNA1D Antibodies:
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Mammalian Monoclonal CACNA1D Primary Antibody for ISt, IHC - ABIN1304578
Bernstein, Guo, Peterson, Wistow: Expressed sequence tag analysis of adult human optic nerve for NEIBank: identification of cell type and tissue markers. in BMC neuroscience 2009
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Mammalian Monoclonal CACNA1D Primary Antibody for ISt, IHC - ABIN1304579
Lu, Sirish, Zhang, Woltz, Li, Timofeyev, Knowlton, Zhang, Yamoah, Chiamvimonvat: Regulation of gene transcription by voltage-gated L-type calcium channel, Cav1.3. in The Journal of biological chemistry 2015
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Human Polyclonal CACNA1D Primary Antibody for IHC, IHC (p) - ABIN4288314
Scholl, Goh, Stölting, de Oliveira, Choi, Overton, Fonseca, Korah, Starker, Kunstman, Prasad, Hartung, Mauras, Benson, Brady, Shapiro, Loring, Nelson-Williams, Libutti, Mane, Hellman, Westin et al.: Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism. ... in Nature genetics 2013
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Human Polyclonal CACNA1D Primary Antibody for IF (p), IHC (p) - ABIN751333
Lobeck, Donnelly, Dupree, Mahe, McNeal, Mohanty, Tiao: Rhesus rotavirus VP6 regulates ERK-dependent calcium influx in cholangiocytes. in Virology 2016
Mouse (Murine) Polyclonal CACNA1D Primary Antibody for WB - ABIN3043768
Guo, Cui, Jiang, Zhang, Jiang: Proteomics of acute heart failure in a rat post-myocardial infarction model. in Molecular medicine reports 2018
Mutations in zebrafish cav1.3a underlie the auditory-vestibular defects of gemini (gem) circler mutants. gem mutant hair cells display normal cell viability, afferent synaptogenesis, and peripheral innervation, yet exhibit reduced extracellular potentials
Adrenal fasciculata cells express Cav1.3 and Cav3.2 calcium channels that regulate cortisol secretion.
new information on the hypothalamic expression of alpha1A and alpha1D subunits during development in a mammal with a long gestation period and a large and convoluted brain.
new findings together with previously published data allow classification of pathogenic CACNA1D mutations into four categories based on prototypical functional changes
alpha1D is involved in the regulation of Ca(2+) homeostasis and cell migration by a mechanism independent of its plasma membrane canonical function but that involved plasma membrane Na(+)/Ca(2+) exchanger
Next-generation sequencing of DNA from Idiopathic Hyperaldosteronism Aldosterone-producing cell cluster demonstrated high prevalence of mutations in the CACNA1D L-type calcium channel.
results reveal a critical extracellular determinant of current density for all Cav family members and of voltage-dependent inactivation of Cav1.3 and Cav2.1 channels
CACNA1D mutation is associated with sinoatrial node dysfunction and deafness .
Although both otoferlin and synaptotagmin bind membrane fusion SNARE proteins, only otoferlin interacts with the L-type calcium channel Cav1.3.
Study have showned a significant effect of the autism-associated mutation A760G on the gating of CaV1.3 such that channel activation is significantly left-shifted, Ca(2+)-dependent inactivation is decreased, and deactivation is slowed, resulting in excess Ca2+ entry. However, these effects are mitigated by an increase in voltage-dependent inactivation. Also, A760G mutation differentially affects CaV1.3 splice variants.
Data suggest that p.G403D mutation in CACNA1D causes persistent hyperinsulinaemic hypoglycaemia with heart defects (presenting as aortic valve insufficiency) and severe neuromuscular disease (presenting as hypotonia); this study involves DNA mutational analysis in one patient plus 2 unrelated patients. [CASE REPORT]
These results provide the evidence of a direct regulatory role of Snapin on Cav1.3 channels in atrial myocytes.
Study used structure modeling and MD simulations to predict omega-currents in CaV1.1 and CaV1.3 channel VSDs when one of the first three S4 gating charges harbors a disease-causing mutation. Using site-directed mutagenesis and electrophysiology, experimentally confirmed that the mutation of R3 charge to His in VSD III of CaV1.3 channels results in an omega-current at hyperpolarizing potentials.
CACNA1D mutations predominate in small zona glomerulosa (ZG)-like Aldosterone-producing Adenomas.
The CACNA1C-L762F mutation is associated with development of long QT syndrome through slower channel inactivation and increased sustained and window current. Timothy syndrome -associated mutations localize to specific areas of CACNA1C and are associated with a younger age at presentation, higher QTc, and 2:1 AV block than isolated LQTS-associated mutations.
Mutations in CACNA1D cause the excessive autonomous aldosterone secretion of Aldosterone-producing Adenomas.
While the relative contribution of Cav1.3 to intestinal Ca(2+) absorption and its value as a therapeutic target remain to be established, we postulate that Cav1.3 downregulation in IBD may contribute to the negative systemic Ca(2+) balance, to increased bone resorption, and to reduced bone mineral density in IBD patients.
E2 upregulated the expression of Cav1.3 for Ca2+ influx to promote the expression of p-ERK1/2 for cell proliferation in breast cancer cells
LRP1B, BRD2 and CACNA1D are new candidate genes in fetal metabolic programming of newborns exposed to maternal hyperglycemia.
CACNA1D might not be a risk gene for SCZ in Han Chinese population, which add to the current state of knowledge regarding the susceptibility of CACNA1D to schizophrenia.
patients with CACNA1D mutations displayed characteristics similar to wild-type aldosterone-producing adenomas
Studies indicate the function of L-type calcium channels Cav1.3 in chromaffin cells.
Studies indicate a role for L-type calcium channel Cav1.3 and Cav1.4 in cochlear inner hair cells (IHCs) and retinal photoreceptors (PRs).
Data show that editing of Cav1.3 calcium channel (CaV1.3) was potently inhibited by serine/arginine-rich splicing factor 9 (SRSF9).
The molecular interactions engaging D4 in VSD IV contribute to voltage-sensing in all examined CaV1.3 channel, however its striking role in regulating the gating properties by alternative splicing appears to be a unique property of the skeletal muscle CaV1.1 channel.
This study showed that Cav1.3 channels promote type-1 cell proliferation, neuronal fate choice, and subsequent neuronal differentiation. Cav1.3 channels expressed on type-1 cells
The results signify a developmental decline in the sensitivity of CDI to global elevations in Ca ( 2+) , which restricts negative feedback regulation of Cav 1.3 channels to incoming Ca ( 2+) ions in mature inner hair cells (IHCs).
Ventral tegmental area Cav1.3 channel activation robustly mediates cocaine-related, depression-related and social behavior via distinct nucleus accumbens AMPAR mechanisms with no effect on anxiety-like behavior.
findings suggest a key role of CaV1.3 in regulating dendritic spine structure. Under physiological conditions it may contribute to the structural plasticity of glutamatergic synapses. Conversely, altered regulation of CaV1.3 channels may provide an important mechanism in the development of postsynaptic aberrations associated with neurodegenerative disorders.
Ca(2+) entry serves critical cellular functions in virtually every cell type, and appropriate regulation of Ca(2+) in neurons is essential for proper function.
Auditory inner hair cells (IHCs) encode sounds into nerve impulses through fast and indefatigable Ca(2+)-dependent exocytosis at their ribbon synapses. We show that this synaptic process involves long and short C-terminal isoforms of the Cav1.3 Ca(2+) channel that differ in the kinetics of their Ca(2+)-dependent inactivation and their relative sensitivity to the l-type Ca(2+) channel blocker nifedipine.
Inner hair cells possess calcium channels that are essential for transmitting sound information into synaptic transmitter release. Voltage-gated calcium channels can coassemble with auxiliary subunit alpha2delta isoforms 1-4. We found that hair cells of the mouse express the auxiliary subunit alpha2delta2, which is needed for normal hearing thresholds. Using a mouse model with a mutant, nonfunctional alpha2delta2 prote...
alpha1D Ca and SK4 channels are coupled in the atria, and deletion of alpha1D leads to decreased SK4 mRNA and BNP secretion providing evidence for a novel role of alpha1D in atrial endocrine function
beta-Adrenergic stimulation enhanced pacemaking of both genotypes, though, Cav1.3(-/-) sino-atrial node cells remained slower than wild type
implicating Cav1.3 as an essential element for hippocampus-associated cognitive functions
Data suggest that the ion channels CaV1.3, bestrophin-1 and maxiK were identified as players in the regulation of photoreceptor outer segments (POS) phagocytosis by the retinal pigment epithelium (RPE).
Cp8 is a new of Cav1.2 and Cav1.3 channel activators.
RIM2alpha and RIM2beta promote a large complement of synaptic CaV1.3 Ca(2+) channels at inner hair cell presynaptic active zones and are required for normal hearing.
Results indicate that the Cav1.3 subtype is crucial to regulation of basal single-spike firing, while activation of both Cav1.2 and Cav1.3 can support burst firing of dopaminergic VTA neurons.
ablation of Cav1.3 results in a decrease in the protein expression of myosin light chain 2, which interacts and increases the membrane localization of SK2 channels.
These data demonstrate that type 1 diabetic serum hyperactivates both CaV1.2 and CaV1.3 channels by increasing their conductivity and number.
Voltage-dependent calcium 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, and gene expression. Calcium channels are multisubunit complexes composed of alpha-1, beta, alpha-2/delta, and gamma subunits. The channel activity is directed by the pore-forming alpha-1 subunit, whereas the others act as auxiliary subunits regulating this activity. The distinctive properties of the calcium channel types are related primarily to the expression of a variety of alpha-1 isoforms, namely alpha-1A, B, C, D, E, and S. This gene encodes the alpha-1D subunit. Several transcript variants encoding different isoforms have been found for this gene.
L-type calcium channel pore subunit isoform 1.3a
, voltage-dependent L-type calcium channel subunit alpha-1D
, voltage-gated calcium channel alpha 1D subunit
, calcium channel, voltage-dependent, L type, alpha 1D subunit
, voltage-gated calcium channel subunit Cav1.3
, calcium channel voltage-dependent L type Cav1.3, alpha 1d subunit
, voltage-dependent L-type calcium channel subunit alpha-1D-like
, calcium channel, L type, alpha-1 polypeptide
, calcium channel, neuroendocrine/brain-type, alpha 1 subunit
, voltage-gated calcium channel alpha 1 subunit
, voltage-gated calcium channel alpha subunit Cav1.3
, brain class D
, calcium channel alpha-1 subunit
, voltage-dependent calcium channel subunit alpha1D
, voltage-gated calcium channel pore forming subunit CaV1.3alpha1 IVS3-IVS4 extracellular linker
, voltage-gated calcium channel subunit alpha Cav1.3
, alpha 1 E
, L-type voltage-gated calcium channel alpha1D subunit ChCaChA1D