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MABC595

Sigma-Aldrich

Anti-VEGF 165b Antibody, clone 56/1

clone 56/1, 1 mg/mL, from mouse

Synonym(s):

Vascular endothelial growth factor 165b, Vascular endothelial growth factor 165, Vascular endothelial growth factor A, Vascular permeability factor

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

56/1, monoclonal

species reactivity

human, mouse, rat

concentration

1 mg/mL

technique(s)

ELISA: suitable
immunohistochemistry: suitable
western blot: suitable

isotype

IgG1κ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... VEGFA(7422)

General description

VEGF (Vascular endothelial growth factor, VEGFA, VEGF-A), a dimeric ligand, is among the most potent angiogenic mitogens. VEGF is secreted by tumor cells and other cells exposed to hypoxia. VEGF is a highly specific mitogen for vascular endothelial cells. Seven VEGF isoforms (a, b, c, d, e, f, g) are generated as a result of alternative splicing from a single VEGF gene. The most commonly studied isoforms are VEGF121, VEGF165, and VEGF189 (f, d and b, respectively) All seven isoforms differ in their molecular mass and in biological properties such as their ability to bind to cell-surface heparan-sulfate proteoglycans. The expression of VEGF is potentiated and is secreted by tumor cells in response to hypoxia, by activated oncogenes, and by a variety of cytokines. VEGF induces angiogenesis as well as permeabilization of blood vessels, and plays a central role in the regulation of vasculogenesis. VEGF expression correlates to the degree of tumor vascularization and with increased metastatic risk. Additionally, VEGF induces endothelial cell proliferation, promotes cell migration, and inhibits apoptosis. Consequently, inhibition of VEGF signaling abrogates the development of a wide variety of tumors.

Immunogen

Epitope: C-terminus
KLH-conjugated linear peptide corresponding to the C-terminus of Mouse VEGF 165b.

Application

Research Category
Apoptosis & Cancer
Research Sub Category
Apoptosis - Additional
This Anti-VEGF 165b Antibody, clone 56/1 is validated for use in Western Blotting and Immunohistochemistry and ELISA for the detection of VEGF 165b.
Western Blotting Analysis: 2 µg/mL of a representative lot of this antibody detected VEGF 165b in 10 µg of PC12 cell lysate.

Immunohistochemistry Analysis: A 1:50 dilution of a representative lot detected detected VEGF 165b in tumor cells of human prostate cancer tissue.

Western Blotting Analysis: A representative lot detected recombinant VEGF 165b protein (Woolard, J., et al. (2004) CANCER RESEARCH 64:7822–7835).

Western Blotting Analysis: A representative lot detected VEGF 165b in human eye tissue lysate (Perrin, R.M., et al. (2005) Diabetologia. 48: 2422–2427).

Immunohistochemistry Analysis: A representative lot detected VEGF 165b in Mouse mesentery tissue (Woolard, J., et al. (2004) CANCER RESEARCH 64:7822–7835).

Immunohistochemistry Analysis: A representative lot detected VEGF 165b in tumor tissue sections (Peiris-Pagès, M., et al. (2010) Pathol. 222(2): 138–147).

ELISA: A representative lot of this antibody detected VEGF 165b by ELISA on tumor tissue samples & tumor cell lines (Peiris-Pagès, M., et al. (2010) Pathol. 222(2): 138–147).

ELISA: A representative lot of this antibody detected VEGF 165b by ELISA on recombinant protein VEGF 165b (Woolard, J., et al. (2004) CANCER RESEARCH 64:7822–7835).

Quality

Evaluated by Western Blotting in NIH/3T3 cell lysate.

Western Blotting Analysis: 2 µg/mL of this antibody detected VEGF 165b in 10 µg of NIH/3T3 cell lysate.

Target description

~ 22 kDa observed.
Additional uncharacterized bands may be visible in some lysates.

Physical form

Format: Purified
Protein G Purified
Purified mouse monoclonal IgG1κ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

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 Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Effects of Therapeutic Platelet-Rich Plasma on Overactive Bladder via Modulating Hyaluronan Synthesis in Ovariectomized Rat.
Lu, et al.
International Journal of Molecular Sciences, 24 (2023)
John M Hatcher et al.
Cell chemical biology, 25(4), 460-470 (2018-02-27)
The SRPK family of kinases regulates pre-mRNA splicing by phosphorylating serine/arginine (SR)-rich splicing factors, signals splicing control in response to extracellular stimuli, and contributes to tumorigenesis, suggesting that these splicing kinases are potential therapeutic targets. Here, we report the development
Kun-Ling Lin et al.
International journal of molecular sciences, 22(17) (2021-09-11)
Postmenopausal women with ovary hormone deficiency (OHD) are subject to overactive bladder (OAB) symptoms. The present study attempted to elucidate whether low-intensity extracorporeal shock wave therapy (LiESWT) alters bladder angiogenesis, decreases inflammatory response, and ameliorates bladder hyperactivity to influence bladder
Liang-Hui Chu et al.
Scientific reports, 6, 37030-37030 (2016-11-18)
Angiogenesis is the growth of new blood vessels from pre-existing microvessels. Peripheral arterial disease (PAD) is caused by atherosclerosis that results in ischemia mostly in the lower extremities. Clinical trials including VEGF-A administration for therapeutic angiogenesis have not been successful.
Jing Li et al.
Frontiers in cellular neuroscience, 11, 381-381 (2017-12-15)
After complete transection of the thoracic spinal segment, neonatal rats exhibit spontaneous locomotor recovery of hindlimbs, but this recovery is not found in adult rats after similar injury. The potential mechanism related to the difference in recovery of neonatal and

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