PROCR anticorps (APC)

N° du produit ABIN2657022

Cet anticorps Rat Monoclonal détecte spécifiquement PROCR dans FACS. Il présente une réactivité envers Souris.

Aperçu rapide pour PROCR anticorps (APC) (ABIN2657022)

Antigène: PROCR (Protein C Receptor, Endothelial (PROCR))

Reactivité: Souris

Hôte: Rat

Clonalité: Monoclonal

Conjugué: Cet anticorp PROCR est conjugé à/à la APC

Application: Flow Cytometry (FACS)

Clone: RCR-16

Détail du produit anti-PROCR anticorps (APC)

Purification: The antibody was purified by affinity chromatography and conjugated with APC under optimal conditions. The solution is free of unconjugated APC and unconjugated antibody.

Isotype: IgG2a kappa

Information d'application

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

Restrictions: For Research Use only

Stockage

Concentration: 0.2 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.

Conseil sur la manipulation: Protect from prolonged exposure to light. Do not freeze.

Stock: 4 °C

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

Détails sur PROCR

Antigène: PROCR (Protein C Receptor, Endothelial (PROCR))

Autre désignation: CD201

Sujet: Endothelial protein C receptor (EPCR), also known as CD201, is a 46 kD N-glycosylated type I transmembrane protein, primarily expressed on the endothelial cells of arteries and veins in heart and lung. It is also expressed at high levels on a subset of hematopoietic stem cells and a subset of dendritic cells. CD201 functions as a primary receptor for protein C activation, and results in inhibition of both intrinsic and extrinsic coagulation pathways. It also plays an important role in many pathophysiologic processes, such as inflammation responses to infection, trauma, hematopoiesis, and autoimmune response. Deletion of the CD201 gene in knock-out mice leads to embryonic lethality before embryonic day 10, indicating that CD201 expression is critical for embryo development. In humans, mutations of CD201 have been associated with venous thromboembolism and myocardial infarction as well as with late fetal loss during pregnancy.