ADAM10 Antikörper

Produktnummer ABIN2664261

Dieser Maus Monoklonal Antikörper erkennt spezifisch ADAM10 in ICFC. Er zeigt eine Reaktivität gegenüber Human.

Kurzübersicht für ADAM10 Antikörper (ABIN2664261)

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

Reaktivität: Human

Wirt: Maus

Klonalität: Monoklonal

Konjugat: Dieser ADAM10 Antikörper ist unkonjugiert

Applikation: Intracellular Flow Cytometry (ICFC)

Klon: SHM14

Produktdetails anti-ADAM10 Antikörper

Aufreinigung: The antibody was purified by affinity chromatography.

Isotyp: IgG1 kappa

Anwendungsinformationen

Applikationshinweise: Optimal working dilution should be determined by the investigator.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Konzentration: 0.5 mg/mL

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

Konservierungsmittel: Sodium azide

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

Lagerung: 4 °C

Informationen zur Lagerung: The antibody solution should be stored undiluted between 2°C and 8°C.

Details zu ADAM10

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

Andere Bezeichnung: CD156c

Hintergrund: 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: Notch Signalweg, EGFR Signaling Pathway