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Mouse Anti-ANK3 Recombinant Antibody (463) (CBMAB-A2756-YC)

Provided herein is a Mouse monoclonal antibody against Mouse Ankyrin 3. The antibody can be used for immunoassay techniques, such as IF, WB.
See all ANK3 antibodies
Published Data

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
463
Antibody Isotype
IgG1, κ
Application
IHC-P, ICC, IF, WB

Basic Information

Immunogen
Synthetic peptide from human ankyrin G spectrin binding protein
Host Species
Mouse
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500
IHC-P1:50-1:500

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Ankyrin 3
Introduction
Ankyrins are a family of proteins that are believed to link the integral membrane proteins to the underlying spectrin-actin cytoskeleton and play key roles in activities such as cell motility, activation, proliferation, contact, and the maintenance of spe
Entrez Gene ID
UniProt ID
Alternative Names
Ankyrin 3; Ankyrin-G; Ankyrin 3, Node Of Ranvier (Ankyrin G); Ankyrin-3, Node Of Ranvier; Ankyrin-3; MRT37; ANK-3;
Function
In skeletal muscle, required for costamere localization of DMD and betaDAG1 (By similarity). Membrane-cytoskeleton linker. May participate in the maintenance/targeting of ion channels and cell adhesion molecules at the nodes of Ranvier and axonal initial segments. Regulates KCNA1 channel activity in function of dietary Mg2+ levels, and thereby contributes to the regulation of renal Mg2+ reabsorption (PubMed:23903368).
Isoform 5: May be part of a Golgi-specific membrane cytoskeleton in association with beta-spectrin.
Biological Process
Axonogenesis Source: BHF-UCL
Cellular response to magnesium ion Source: UniProtKB
Endoplasmic reticulum to Golgi vesicle-mediated transport Source: Reactome
Establishment of protein localization Source: UniProtKB
Golgi to plasma membrane protein transport Source: BHF-UCL
Magnesium ion homeostasis Source: UniProtKB
Maintenance of protein location in plasma membrane Source: BHF-UCL
Membrane assembly Source: BHF-UCL
Mitotic cytokinesis Source: BHF-UCL
Negative regulation of delayed rectifier potassium channel activity Source: UniProtKB
Neuromuscular junction development Source: BHF-UCL
Neuronal action potential Source: BHF-UCL
Plasma membrane organization Source: BHF-UCL
Positive regulation of cation channel activity Source: BHF-UCL
Positive regulation of cell communication by electrical coupling Source: BHF-UCL
Positive regulation of gene expression Source: BHF-UCL
Positive regulation of homotypic cell-cell adhesion Source: BHF-UCL
Positive regulation of membrane depolarization during cardiac muscle cell action potential Source: BHF-UCL
Positive regulation of membrane potential Source: BHF-UCL
Positive regulation of protein targeting to membrane Source: BHF-UCL
Positive regulation of sodium ion transmembrane transporter activity Source: BHF-UCL
Positive regulation of sodium ion transport Source: BHF-UCL
Protein localization to axon Source: UniProtKB
Protein localization to plasma membrane Source: BHF-UCL
Regulation of potassium ion transport Source: BHF-UCL
Signal transduction Source: InterPro
Cellular Location
Sarcolemma; Postsynaptic cell membrane; T-tubule; Cytoskeleton; Lysosome; Axon. In skeletal muscle, localized at costameres and neuromuscular junctions. In macrophages, associated with lysosomes.
Isoform 5: Golgi apparatus; Cytoskeleton
Involvement in disease
Mental retardation, autosomal recessive 37 (MRT37): The disease is caused by variants affecting the gene represented in this entry. A homozygous deletion in ANK3 predicted to result in frameshift and premature truncation, has been shown to be the cause of moderate intellectual disability, an ADHD-like phenotype and behavioral problems in a consanguineous family (PubMed:23390136).A disorder characterized by significantly below average general intellectual functioning associated with impairments in adaptive behavior and manifested during the developmental period. MRT37 patients manifest delayed global development with speech delay, hypotonia, spasticity, and a sleep disorder. Severe behavioral abnormalities include aggression, hyperactivity, and grinding of the teeth.
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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