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Mouse Anti-BVES Recombinant Antibody (3F7) (CBMAB-A0914-LY)


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Summary

Host Animal
Mouse
Specificity
Human, Rat
Clone
3F7
Antibody Isotype
IgG2a, κ
Application
WB, E

Basic Information

Immunogen
BVES (NP_009004, 262 a.a. ~ 360 a.a) partial recombinant protein with GST tag.
Host Species
Mouse
Specificity
Human, Rat
Antibody Isotype
IgG2a, κ
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
Buffer
PBS, pH 7.4
Preservative
None
Concentration
Batch dependent
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
blood vessel epicardial substance
Introduction
This gene encodes a member of the POP family of proteins containing three putative transmembrane domains. This gene is expressed in cardiac and skeletal muscle and may play an important role in development of these tissues. The mouse ortholog may be involved in the regeneration of adult skeletal muscle and may act as a cell adhesion molecule in coronary vasculogenesis. Two transcript variants encoding the same protein have been found for this gene. [provided by RefSeq]
Entrez Gene ID
Human11149
Rat365603
UniProt ID
HumanQ8NE79
RatQ3BCU4
Alternative Names
HBVES; MGC42413; POP1; POPDC1
Function
Cell adhesion molecule involved in the establishment and/or maintenance of cell integrity. Involved in the formation and regulation of the tight junction (TJ) paracellular permeability barrier in epithelial cells (PubMed:16188940).
Plays a role in VAMP3-mediated vesicular transport and recycling of different receptor molecules through its interaction with VAMP3. Plays a role in the regulation of cell shape and movement by modulating the Rho-family GTPase activity through its interaction with ARHGEF25/GEFT. Induces primordial adhesive contact and aggregation of epithelial cells in a Ca2+-independent manner. Also involved in striated muscle regeneration and repair and in the regulation of cell spreading (By similarity).
Important for the maintenance of cardiac function. Plays a regulatory function in heart rate dynamics mediated, at least in part, through cAMP-binding and, probably, by increasing cell surface expression of the potassium channel KCNK2 and enhancing current density (PubMed:26642364).
Is also a caveolae-associated protein important for the preservation of caveolae structural and functional integrity as well as for heart protection against ischemia injury.
Biological Process
Cell migration involved in heart development Source: Ensembl
Epithelial cell-cell adhesion Source: UniProtKB
Heart development Source: UniProtKB
Hematopoietic progenitor cell differentiation Source: Ensembl
Muscle organ development Source: UniProtKB
Positive regulation of locomotion Source: UniProtKB
Positive regulation of receptor recycling Source: UniProtKB
Regulation of cell shape Source: UniProtKB
Regulation of endocytic recycling Source: Ensembl
Regulation of GTPase activity Source: UniProtKB
Regulation of heart rate Source: Ensembl
Regulation of membrane potential Source: GO_Central
Response to ischemia Source: UniProtKB
Sinoatrial node cell development Source: Ensembl
Skeletal muscle tissue development Source: UniProtKB
Striated muscle cell differentiation Source: GO_Central
Substrate adhesion-dependent cell spreading Source: UniProtKB
Vesicle docking Source: Ensembl
Vesicle-mediated transport Source: UniProtKB
Cellular Location
Lateral cell membrane; Sarcolemma; Tight junction; Membrane; Caveola. Colocalizes with VAMP3 at the cell-cell contact in cardiac and skeletal muscle (By similarity). Its movement from the cytoplasm to membrane is an early event occurring concurrently with cell-cell contact. Colocalizes in epithelial cells with OCLN and TJP1 in an apical-lateral position within the z axis. Detected at cell-cell contact but never observed at the free surface of epithelial cells.
Involvement in disease
Muscular dystrophy, limb-girdle, autosomal recessive 25 (LGMDR25): An autosomal recessive muscular disorder characterized by slowly progressive onset of proximal lower limb weakness in adulthood, syncopal episodes, and markedly increased serum creatine kinase, which can increase further after strenuous exercise.
Topology
Extracellular: 1-48 aa
Helical: 49-69 aa
Cytoplasmic: 70 aa
Helical: 71-91 aa
Extracellular: 92 aa
Helical: 93-113 aa
Cytoplasmic: 114-360 aa
More Infomation

Wen, W., Wang, H., Xie, S., Wu, Z., & Zhang, C. (2021). BVES‐AS1 inhibits the malignant behaviors of colon adenocarcinoma cells via regulating BVES. Cell Biology International.

Beecher, G., Tang, C., & Liewluck, T. (2021). Severe adolescent-onset limb-girdle muscular dystrophy due to a novel homozygous nonsense BVES mutation (1497).

Shi, Y., Li, Y., Wang, Y., Zhuang, J., Wang, H., Hu, M., ... & Yuan, W. (2019). The functional polymorphism R129W in the BVES gene is associated with sporadic tetralogy of Fallot in the Han Chinese population. Genetic testing and molecular biomarkers, 23(9), 601-609.

Thompson, J. J., Short, S. P., Parang, B., Brown, R. E., Li, C., Ng, V. H., ... & Williams, C. S. (2019). Blood vessel epicardial substance reduces LRP6 receptor and cytoplasmic β-catenin levels to modulate Wnt signaling and intestinal homeostasis. Carcinogenesis, 40(9), 1086-1098.

Thompson, J. J. (2019). Blood vessel epicardial substance (BVES) and BVES binding partners in intestinal homeostasis and tumorigenesis (Doctoral dissertation).

Han, P., Lei, Y., Li, D., Liu, J., Yan, W., & Tian, D. (2019). Ten years of research on the role of BVES/POPDC1 in human disease: A review. OncoTargets and therapy, 12, 1279.

Parang, B., Thompson, J. J., & Williams, C. S. (2018). Blood Vessel Epicardial Substance (BVES) in junctional signaling and cancer. Tissue Barriers, 6(4), 1-12.

SHI, C. (2018). Expression of BVES in gallbladder carcinoma and inhibitory effects of its overexpression on proliferation and invasion of gallbladder carcinoma cells. Tumor, 958-964.

Parang, B., Kaz, A. M., Barrett, C. W., Short, S. P., Ning, W., Keating, C. E., ... & Williams, C. S. (2017). BVES regulates c-Myc stability via PP2A and suppresses colitis-induced tumourigenesis. Gut, 66(5), 852-862.

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

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