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Mammalian Monoclonal CACNB2 Primary Antibody für ISt, IHC - ABIN1304588
Abiria, Colbran: CaMKII associates with CaV1.2 L-type calcium channels via selected beta subunits to enhance regulatory phosphorylation. in Journal of neurochemistry 2010
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Human Monoclonal CACNB2 Primary Antibody für ELISA, WB - ABIN560146
Horiuchi-Hirose, Kashihara, Nakada, Kurebayashi, Shimojo, Shibazaki, Sheng, Yano, Hirose, Hongo, Sakurai, Moriizumi, Ueda, Yamada: Decrease in the density of t-tubular L-type Ca2+ channel currents in failing ventricular myocytes. in American journal of physiology. Heart and circulatory physiology 2011
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Human Polyclonal CACNB2 Primary Antibody für ELISA, WB - ABIN4286783
Burashnikov, Pfeiffer, Barajas-Martinez, Delpón, Hu, Desai, Borggrefe, Häissaguerre, Kanter, Pollevick, Guerchicoff, Laiño, Marieb, Nademanee, Nam, Robles, Schimpf, Stapleton, Viskin, Winters et al.: Mutations in the cardiac L-type calcium channel associated with inherited J-wave syndromes and sudden cardiac death. ... in Heart rhythm : the official journal of the Heart Rhythm Society 2010
This genotype/phenotype association study uncovered a variant in CACNB2 that may be associated with both KD susceptibility and bifid T waves, a novel signature of altered myocardial repolarization.
Data show that an indispensable beta-subunit of the voltage-gated Ca(2+) channel Cav1.2 interaction with H-Ras is independently of Ca(2+) flux, suggesting the regulatory role of beta2 in transcriptional activation via the ERK/CREB pathway.
Our study shows that palmitoylation of CaVbeta2a is necessary for CaValpha1 trafficking to the plasma membrane. However, excessive number of palmitoylated CaVbeta2a leads to Ca(2+) overload and beta cell death.
Study showed that CACNB2 is a possible candidate hypertrophy-modifying gene contributing to disease variability of MYBPC3-associated familial hypertrophic cardiomyopathy
Five serious mental disorders and three major cardiovascular diseases have recently been linked to the CACNB2 gene coding for the Cavbeta2 subunits
ADM genotype AA was associated with the highest values of systolic and diastolic blood pressure (BP), while CACNB2 genotype CC carriers had the highest values of diastolic BP in childhood.
In the gene-based analysis, CACNB2 and CTCF showed the strongest evidence for association with schizophrenia in both the present samples and in those of the Psychiatric Genetics Consortium datasets.
Chronic atrial fibrillation increases miR-21 expression in human atrial myocytes and decreases I(Ca,L) density by downregulating CACNA1C/CACNB2 expression.
Three rare missense mutations of CACNB2 (G167S, S197F, and F240L) found in Autism Spectrum Disorders (ASD)-affected families, are reported.
High prevalence of CACNA2D1, SCN5A, and CACNB2 genetic variants in the Danish population previously associated with Brugada syndrome has been found in new exome data.
Association of the SNP rs2932538 in MOV10 and SNP rs4373814 in CACNB2 with an increased risk of hypertension in a Chinese Han population.
Genetic variations in CYP17A1, CACNB2 and PLEKHA7 were related to blood pressure traits and/or hypertension in Chinese She population.
Genetic testing reveals disease-causing mutations in depolarizing sodium (SCN5A) or calcium (CaCNB2b) channels in 5 infants with rapid ventricular tachycardia, conduction abnormalities, and Brugada-like syndrome.
This study provided that cacnb2 are associated with Bipolar I in the Han Chinese population.
that genetic variation within CACNB2 may influence treatment-related outcomes in high-risk patients with hypertension.
CACNB2 is a possible novel early repolarization syndrome susceptibility gene.
We also identified a novel polymorphism (D601E) in CACNB2b that slowed inactivation of L-type calcium current (I(Ca,L)), significantly increased total charge. Slowed conduction was present.
loss-of-function mutations in genes encoding the cardiac L-type calcium channel to be associated with a familial sudden cardiac death syndrome in which a Brugada syndrome phenotype is combined with shorter-than-normal QT intervals
Functional properties of the CaV1.2 calcium channel activated by calmodulin in the absence of alpha2delta subunits.
CACNB2 SNPs show genotypic association with Alzheimer disease.
L-type Ca2+ channels in the caveolae microdomain do not affect cardiac function and are not necessary for the regulation of hypertrophic signaling in the adult mouse heart.
Many hormone- or neurotransmitter-activated receptors stimulate PIP2 hydrolysis and increase cytosolic Ca(2+); thus, our findings suggest that beta2e may integrate such receptor-mediated signals to limit Cav activity.
Membrane Interaction of the beta2e Subunit of Voltage-Gated Ca(2+) Channels
Dynamic phospholipid interaction of beta2e subunit regulates the gating of voltage-gated Ca2+ channels.
a model in which CaVbeta promotes anterograde trafficking of the L-type channels by anchoring them to actin filaments in their itinerary to the plasma membrane.
We conclude that phosphorylation of the C-terminal sites in Ca(v)beta(2), Ser(1928), Ser(1512), and Ser(1570) of the Ca(v)1.2 protein is functionally not involved in the adrenergic regulation of the murine cardiac Ca(v)1.2 channel.
phosphorylation event is one mechanism underlying ahnak1's modulator function on Cav1.2 channel activity.
Ca(V)beta2 appears to be a much stronger modulator of L-type calcium currents in embryonic than in adult cardiomyocytes
Mice with cardiac-specific sequestration of the beta-subunit of the L-type calcium channel
L-type calcium channel beta 2 and 4 subunits may play a major role in conferring calcium handling heterogeneity within the developing embryonic myocardium
preferential binding between Cacna1c and Cacnb2 in the heart
Ca(V)beta(2) has an essential role in regulating the abundance and properties of Ca(V)1.3 channels in IHCs and, thereby, is critical for IHC development and synaptic encoding of sound.
expression of various CaVbeta2 proteins may be used to adapt the properties of LTCCs to changing myocardial requirements during development
These studies refine the understanding of beta2 subunit diversity arising from alternative splicing, and provide the groundwork for functional analysis of beta2 subunit diversity in the embryonic heart.
This gene encodes a subunit of a voltage-dependent calcium channel protein that is a member of the voltage-gated calcium channel superfamily. The gene product was originally identified as an antigen target in Lambert-Eaton myasthenic syndrome, an autoimmune disorder. Mutations in this gene are associated with Brugada syndrome. Alternatively spliced variants encoding different isoforms have been described.
, calcium channel voltage-dependent subunit beta 2
, lambert-Eaton myasthenic syndrome antigen B
, myasthenic (Lambert-Eaton) syndrome antigen B
, voltage-dependent L-type calcium channel subunit beta-2
, cardiac calcium channel beta subunit
, cardiac calcium channel beta-subunit
, calcium channel, voltage-dependent, beta 2 subunit
, L-type calcium channel beta subunit
, voltage-dependent L-type calcium channel subunit beta-2-like
, calcium channel, voltage-dependent, beta 2b