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V9263

Sigma-Aldrich

Monoclonal Anti-Vascular Cell Adhesion Molecule 1 antibody produced in mouse

~1 mg/mL, clone 1.4C3, purified immunoglobulin, buffered aqueous solution

Synonym(s):

Anti-VCAM-1

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

1.4C3, monoclonal

form

buffered aqueous solution

mol wt

antigen 110 kDa

species reactivity

human

concentration

~1 mg/mL

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 2-4 μg/mL using human tonsil tissue
immunohistochemistry (frozen sections): 2-4 μg/mL using human tonsil tissue
western blot: suitable

isotype

IgG1

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... VCAM1(7412)

General description

VCAM-1(Vascular Cell Adhesion Molecule-1) belongs to immunoglobulin-related gene superfamily of adhesion molecules and is a 110kD cell surface integral membrane glycoprotein. It is expressed mainly by cytokine-activated endothelium and plays a pivotal role in numerous immunological and inflammatory responses. Monoclonal anti-vascular cell adhesion molecule 1 antibody can be used in immunohistochemistry for formalin-fixed, paraffin-embedded tissue sections. Mouse anti-vascular cell adhesion molecule 1 antibody reacts specifically with human vascular cell adhesion molecule-1 (CD106 or INCAM-110).

Immunogen

stimulated HUVEC cells and mouse NS1 cells.

Application

Monoclonal anti-vascular cell adhesion molecule 1 antibody can be used in immunoblotting and western blotting.

Physical form

Solution in phosphate buffered saline containing 0.08% sodium azide.

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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flash_point_c

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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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Kumiko Nishimura et al.
Life sciences, 203, 276-281 (2018-04-24)
Type 3 iodothyronine deiodinase (D3), which converts thyroxine (T4) and 3,5,3'-triiodothyronine (T3) to 3,3',5'-triiodothyronine (rT3) and 3,3'-diiodothyronine (T2), respectively, inactivates thyroid hormones. We investigated the expression and regulation of D3 in human cardiomyocytes which were differentiated from human induced pluripotent
Darren G Woodside et al.
Journal of immunology (Baltimore, Md. : 1950), 176(8), 5041-5049 (2006-04-06)
Cell adhesion mediated by the interaction between integrin alpha4beta1 and VCAM-1 is important in normal physiologic processes and in inflammatory and autoimmune disease. Numerous studies have mapped the alpha4beta1 binding sites in VCAM-1 that mediate cell adhesion; however, little is
A G Kumar et al.
Journal of immunology (Baltimore, Md. : 1950), 153(9), 4088-4098 (1994-11-01)
Vascular cell adhesion molecule-1 (VCAM-1) is a member of the Ig superfamily that shows increased expression in a number of pathologic conditions. The role of VCAM-1 in human disease remains undefined and murine models are being extensively studied to help
Chengjie Ma et al.
Molecular medicine reports, 22(1), 483-493 (2020-04-23)
Inactivation of the Hippo pathway protects the myocardium from cardiac ischemic injury. MicroRNAs (miRs) have been reported to play pivotal roles in the progression of myocardial infarction (MI). The present study examined whether miR‑93 could promote angiogenesis and attenuate remodeling
Elaine K Gregory et al.
American journal of physiology. Heart and circulatory physiology, 307(10), H1419-H1429 (2014-09-23)
Oral all-trans retinoic acid (atRA) has been shown to reduce the formation of neointimal hyperplasia; however, the dose required was 30 times the chemotherapeutic dose, which already has reported side effects. As neointimal formation is a localized process, new approaches

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