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Mouse Anti-CASQ2 Recombinant Antibody (CBFYC-0864) (CBMAB-C0919-FY)

This product is mouse antibody that recognizes CASQ2. The antibody CBFYC-0864 can be used for immunoassay techniques such as: ELISA, WB, IHC.
See all CASQ2 antibodies

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Pig, Rat
Clone
CBFYC-0864
Antibody Isotype
IgG2a
Application
ELISA, WB, IHC

Basic Information

Specificity
Human, Mouse, Pig, Rat
Antibody Isotype
IgG2a
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

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

Format
Liquid
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
Calsequestrin 2
Introduction
The protein encoded by this gene specifies the cardiac muscle family member of the calsequestrin family. Calsequestrin is localized to the sarcoplasmic reticulum in cardiac and slow skeletal muscle cells. The protein is a calcium binding protein that stores calcium for muscle function. Mutations in this gene cause stress-induced polymorphic ventricular tachycardia, also referred to as catecholaminergic polymorphic ventricular tachycardia 2 (CPVT2), a disease characterized by bidirectional ventricular tachycardia that may lead to cardiac arrest.
Entrez Gene ID
Human845
Mouse12373
Rat29209
Pig397436
UniProt ID
HumanO14958
MouseO09161
RatP51868
PigF1SAW8
Alternative Names
Calsequestrin 2; Calsequestrin, Cardiac Muscle Isoform; Calsequestrin 2 (Cardiac Muscle); Calsequestrin 2, Fast-Twitch, Cardiac Muscle; Calsequestrin-2; PDIB2
Function
Calsequestrin is a high-capacity, moderate affinity, calcium-binding protein and thus acts as an internal calcium store in muscle. Calcium ions are bound by clusters of acidic residues at the protein surface, especially at the interface between subunits. Can bind around 60 Ca2+ ions. Regulates the release of lumenal Ca2+ via the calcium release channel RYR2; this plays an important role in triggering muscle contraction. Plays a role in excitation-contraction coupling in the heart and in regulating the rate of heart beats.
Biological Process
Cardiac muscle contraction Source: BHF-UCL
Cellular response to caffeine Source: BHF-UCL
Detection of calcium ion Source: BHF-UCL
Ion transmembrane transport Source: Reactome
Negative regulation of potassium ion transmembrane transporter activity Source: BHF-UCL
Negative regulation of potassium ion transport Source: BHF-UCL
Negative regulation of ryanodine-sensitive calcium-release channel activity Source: BHF-UCL
Protein polymerization Source: UniProtKB
Purkinje myocyte to ventricular cardiac muscle cell signaling Source: BHF-UCL
Regulation of cardiac conduction Source: Reactome
Regulation of cardiac muscle contraction by regulation of the release of sequestered calcium ion Source: BHF-UCL
Regulation of cell communication by electrical coupling Source: BHF-UCL
Regulation of heart rate Source: UniProtKB
Regulation of membrane repolarization Source: BHF-UCL
Regulation of release of sequestered calcium ion into cytosol Source: GO_Central
Regulation of release of sequestered calcium ion into cytosol by sarcoplasmic reticulum Source: BHF-UCL
Sequestering of calcium ion Source: BHF-UCL
Striated muscle contraction Source: ProtInc
Cellular Location
Sarcoplasmic reticulum lumen. This isoform of calsequestrin occurs in the sarcoplasmic reticulum's terminal cisternae luminal spaces of cardiac and slow skeletal muscle cells.
Involvement in disease
Ventricular tachycardia, catecholaminergic polymorphic, 2 (CPVT2): An arrhythmogenic disorder characterized by stress-induced, bidirectional ventricular tachycardia that may degenerate into cardiac arrest and cause sudden death. Patients present with recurrent syncope, seizures, or sudden death after physical activity or emotional stress. CPVT2 inheritance is autosomal recessive.
PTM
Phosphorylation in the C-terminus, probably by CK2, moderately increases calcium buffering capacity.
N-glycosylated.

Kim, J. H., Lee, E. S., Yun, J., Ryu, H. S., Kim, H. K., Ju, Y. W., ... & Moon, H. G. (2021). Calsequestrin 2 overexpression in breast cancer increases tumorigenesis and metastasis by modulating the tumor microenvironment. Molecular Oncology.

Valle, G., Arad, M., & Volpe, P. (2020). Molecular adaptation to calsequestrin 2 (CASQ2) point mutations leading to catecholaminergic polymorphic ventricular tachycardia (CPVT): comparative analysis of R33Q and D307H mutants. Journal of muscle research and cell motility, 41(2), 251-258.

Ross, S., Holliday, M., Lim, S., & Semsarian, C. (2019). Characterization of the first induced pluripotent stem cell line generated from a patient with autosomal dominant catecholaminergic polymorphic ventricular tachycardia due to a heterozygous mutation in cardiac calsequestrin-2. Stem cell research, 37, 101450.

Kim, J. H., sil Hong, B., Heo, W., Han, J. M., Han, W., Noh, D. Y., & Moon, H. G. (2018). Calsequestrin 2 regulates proliferation, migration, and invasion in triple-negative breast cancer cells.

Rebrova, T. Y., Muslimova, E. F., Kondratieva, D. S., Budnikova, O. V., Ahmedov, S. D., Afanasiev, S. A., & Popov, S. V. (2018). The Role of Ca 2+-ATPase 2a (ATP2A2), Ryanodine Receptors (RYR2), and Calsequestrin (CASQ2) Gene Polymorphisms in the Development of Heart Failure. Russian Journal of Genetics, 54(6), 604-608.

Josephs, K., Patel, K., Janson, C. M., Montagna, C., & McDonald, T. V. (2017). Compound heterozygous CASQ 2 mutations and long‐term course of catecholaminergic polymorphic ventricular tachycardia. Molecular genetics & genomic medicine, 5(6), 788-794.

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For research use only. Not intended for any clinical use.

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