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Anti-CaV1.3 Mouse Antibody [G19D14]

Catalog No.: F3798

Application: Reactivity: Human, Mouse

Usage Information

Dilution
IHC1:100

Application
IHC, FCM

Reactivity
Human, Mouse

Source
Mouse

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Positive Control	Human hippocampus; Mouse backskin; SH-SY5Y
Negative Control

Datasheet & SDS

Biological Description

Specificity
CaV1.3 Mouse mAb detects endogenous levels of total CaV1.3 protein.

Clone
G19D14

Synonym(s)
CACH3, CACN4, CACNL1A2, CCHL1A2, CACNA1D, Voltage-dependent L-type calcium channel subunit alpha-1D, Voltage-gated calcium channel subunit alpha Cav1.3.

Background
Cardiac excitation–contraction coupling refers to the sequence of events in which electrical stimulation of a cardiomyocyte triggers muscle contraction in the heart. L-type Ca²⁺ channels are critical to this process, as they facilitate calcium influx and contribute to membrane excitability. Four L-type Ca²⁺ channel subtypes have been identified: Cav1.1, Cav1.2, Cav1.3, and Cav1.4. Cav1.1 is predominantly found in skeletal muscle, while Cav1.4 is mainly expressed in the retina and certain immune cells. Cav1.3 is present in the heart, somatodendritic regions of neurons, endocrine cells, and sensory cells. In the heart, Cav1.3 activity is modulated by multiple neurotransmitters. Phosphorylation by cAMP-dependent protein kinase A (PKA) occurs at serine residues 1743 and 1816 within the C-terminal region. Protein kinase C (PKC) also regulates Cav1.3 in an isozyme-specific manner via phosphorylation at serine 81 in the N-terminal domain. Additionally, alternative splicing within the C-terminus influences channel behavior, notably decreasing Ca²⁺-dependent inactivation. Functionally, Cav1.3 contributes to cardiac pacemaking and atrioventricular (AV) conduction. Dysfunction of Cav1.3 has been associated with sinoatrial node and AV node abnormalities, as well as the development of atrial fibrillation.

Background

Cardiac excitation–contraction coupling refers to the sequence of events in which electrical stimulation of a cardiomyocyte triggers muscle contraction in the heart. L-type Ca²⁺ channels are critical to this process, as they facilitate calcium influx and contribute to membrane excitability. Four L-type Ca²⁺ channel subtypes have been identified: Cav1.1, Cav1.2, Cav1.3, and Cav1.4. Cav1.1 is predominantly found in skeletal muscle, while Cav1.4 is mainly expressed in the retina and certain immune cells. Cav1.3 is present in the heart, somatodendritic regions of neurons, endocrine cells, and sensory cells. In the heart, Cav1.3 activity is modulated by multiple neurotransmitters. Phosphorylation by cAMP-dependent protein kinase A (PKA) occurs at serine residues 1743 and 1816 within the C-terminal region. Protein kinase C (PKC) also regulates Cav1.3 in an isozyme-specific manner via phosphorylation at serine 81 in the N-terminal domain. Additionally, alternative splicing within the C-terminus influences channel behavior, notably decreasing Ca²⁺-dependent inactivation. Functionally, Cav1.3 contributes to cardiac pacemaking and atrioventricular (AV) conduction. Dysfunction of Cav1.3 has been associated with sinoatrial node and AV node abnormalities, as well as the development of atrial fibrillation.

References
https://pubmed.ncbi.nlm.nih.gov/37025382/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%