HPA014788
Anti-BVES antibody produced in rabbit
Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Sinónimos:
Anti-Blood vessel epicardial substance, Anti-Popeye domain-containing protein 1, Anti-Popeye protein 1, Anti-hBVES
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About This Item
Productos recomendados
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
product line
Prestige Antibodies® Powered by Atlas Antibodies
form
buffered aqueous glycerol solution
species reactivity
human
enhanced validation
orthogonal RNAseq
Learn more about Antibody Enhanced Validation
technique(s)
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:50-1:200
immunogen sequence
LNDPTLNDKKAKKLEHQLSLCTQISMLEMRNSIASSSDSDDGLHQFLRGTSSMSSLHVSSPHQRASAKMKPIEEGAEDDDDVFEPASPNTLKVHQLP
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... BVES(11149)
General description
BVES (blood vessel epicardial substance) is the prototypic member of Popeye Domain Containing (Popdc) family, and is also called POPDC1. This family has two other members called POPDC2 and POPDC3. BVES is a transmembrane epithelial adhesion protein, containing the characteristic Popeye domain made of amino acids 172-266. It spans the membrane 3 times, and its C-terminal faces the cytoplasm. Homotypic interaction of BVES-BVES is essential for its localization to plasma membrane. It was initially identified in the cDNA library of developing heart.
Immunogen
Blood vessel epicardial substance recombinant protein epitope signature tag (PrEST)
Application
All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.
The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.
The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.
Biochem/physiol Actions
BVES (blood vessel epicardial substance) is involved in the control of tight junction formation in epithelial cells. These tight junctions in turn control RhoA and ZONAB/DbpA, which is a y-box transcription factor. Therefore, the expression and residence of BVES has a regulatory effect on RhoA and ZONAB/DbpA activity. Suppression of this protein leads to DNA hypermethylation or the silencing of transcription. It is down-regulated in all stages of human colorectal carcinoma (CRC) and in adenomatous polyps. Its down-regulation is associated with epithelial-mesenchymal transition (EMT), and consequent colon tumorigenesis. BVES is also down-regulated in gastric cancer, and this is associated with enhanced tumorigenesis and poor patient prognosis. This protein is a key player in the development of embryo and cardiocyte differentiation. It is over-expressed in patients with congenital defects of septa and is linked with tetralogy of Fallot (TOF).
Features and Benefits
Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.
Every Prestige Antibody is tested in the following ways:
Every Prestige Antibody is tested in the following ways:
- IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
- Protein array of 364 human recombinant protein fragments.
Linkage
Corresponding Antigen APREST73021
Physical form
Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide
Legal Information
Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class
10 - Combustible liquids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
Certificados de análisis (COA)
Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»
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Encuentre la documentación para los productos que ha comprado recientemente en la Biblioteca de documentos.
Willem De Ridder et al.
Neurology. Genetics, 5(2), e321-e321 (2019-05-24)
To study the genetic and phenotypic spectrum of patients harboring recessive mutations in BVES. We performed whole-exome sequencing in a multicenter cohort of 1929 patients with a suspected hereditary myopathy, showing unexplained limb-girdle muscular weakness and/or elevated creatine kinase levels.
Min Wu et al.
International journal of molecular medicine, 31(4), 899-903 (2013-02-14)
Tetralogy of Fallot (TOF) is a common congenital heart defect (CHD). However, the genetic causes are largely unknown. Blood vessel epicardial substance (BVES) is postulated to play a role in embryonic development, and we previously found that the expression of
Tanya A Baldwin et al.
EMBO reports, 23(12), e55208-e55208 (2022-10-19)
The establishment of macromolecular complexes by scaffolding proteins is key to the local production of cAMP by anchored adenylyl cyclase (AC) and the subsequent cAMP signaling necessary for cardiac functions. We identify a novel AC scaffold, the Popeye domain-containing (POPDC)
Deng Luo et al.
Pathology oncology research : POR, 18(2), 491-497 (2011-11-24)
Although many molecular and biological studies have shown risk factors for gastric cancer, the available knowledge is still insufficient to unveil the exact mechanism of gastric cancer. To investigate the relationships between Bves expression and the clinicopathologic features of gastric
Haiwen Li et al.
Molecular therapy : the journal of the American Society of Gene Therapy, 31(2), 398-408 (2022-11-27)
Limb-girdle muscular dystrophy type R25 (LGMDR25) is caused by recessive mutations in BVES encoding a cAMP-binding protein, characterized by progressive muscular dystrophy with deteriorating muscle function and impaired cardiac conduction in patients. There is currently no therapeutic treatment for LGMDR25
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