ADAM10 anticorps

N° du produit ABIN2664261

Cet anticorps Souris Monoclonal détecte spécifiquement ADAM10 dans ICFC. Il présente une réactivité envers Humain.

Aperçu rapide pour ADAM10 anticorps (ABIN2664261)

Antigène: ADAM10 (ADAM Metallopeptidase Domain 10 (ADAM10))

Reactivité: Humain

Hôte: Souris

Clonalité: Monoclonal

Conjugué: Cet anticorp ADAM10 est non-conjugé

Application: Intracellular Flow Cytometry (ICFC)

Clone: SHM14

Détail du produit anti-ADAM10 anticorps

Purification: The antibody was purified by affinity chromatography.

Isotype: IgG1 kappa

Information d'application

Indications d'application: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Stockage

Concentration: 0.5 mg/mL

Buffer: Phosphate-buffered solution, pH 7.2, containing 0.09 % sodium azide.

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Stock: 4 °C

Stockage commentaire: The antibody solution should be stored undiluted between 2°C and 8°C.

Détails sur ADAM10

Antigène: ADAM10 (ADAM Metallopeptidase Domain 10 (ADAM10))

Autre désignation: CD156c

Sujet: CD156c, also known as a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10), is a 748 amino acid type I membrane glycoprotein ubiquitously expressed on most cell types. It consists of multiple functional domains, including a N-terminal prodomain, catalytic domain, cysteine-rich domain, transmembranous domain, and cytoplasmic domain. It is secreted as a precursor protein and becomes as the activate/mature form through removing the ADAM10 prodomain by proprotein convertase 7 and furin. ADAM10 functions as metalloproteinase to cleave several molecules including Notch, pro-TNF-α, amyloid precursor protein, myelin basic protein, and type IV collagen. It mediates the release of several cell adhesion molecules such as vascular endothelial cadherin or L-selectin to regulate endothelial permeability and leukocyte transmigration. Dysregulation of ADAM activity may contribute to the pathogenesis of vascular diseases.

Pathways: Signalisation Notch, EGFR Signaling Pathway