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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

Sinônimo(s):

Anti-VCAM-1

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About This Item

Número MDL:
Código UNSPSC:
12352203
NACRES:
NA.41

fonte biológica

mouse

Nível de qualidade

conjugado

unconjugated

forma do anticorpo

purified immunoglobulin

tipo de produto de anticorpo

primary antibodies

clone

1.4C3, monoclonal

forma

buffered aqueous solution

peso molecular

antigen 110 kDa

reatividade de espécies

human

concentração

~1 mg/mL

técnica(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

Isotipo

IgG1

nº de adesão UniProt

Condições de expedição

wet ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... VCAM1(7412)

Descrição geral

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).

Imunogênio

stimulated HUVEC cells and mouse NS1 cells.

Aplicação

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

forma física

Solution in phosphate buffered saline containing 0.08% sodium azide.

Exoneração de responsabilidade

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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Código de classe de armazenamento

12 - Non Combustible Liquids

Classe de risco de água (WGK)

WGK 2

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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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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