PROCR antibody (PE)

Catalog No. ABIN2662525

The Rat Monoclonal anti-PROCR antibody has been validated for IP, ELISA (Capture) and ELISpot. It is suitable to detect PROCR in samples from Mouse.

Quick Overview for PROCR antibody (PE) (ABIN2662525)

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

Reactivity: Mouse

Host: Rat

Clonality: Monoclonal

Conjugate: This PROCR antibody is conjugated to PE

Application: Immunoprecipitation (IP), ELISA (Capture), ELISpot

Clone: RCR-16

Product Details anti-PROCR Antibody (PE)

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

Isotype: IgG2a kappa

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

Concentration: 0.2 mg/mL

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

Preservative: Sodium azide

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

Handling Advice: Protect from prolonged exposure to light. Do not freeze.

Storage: 4 °C

Storage Comment: The antibody solution should be stored undiluted between 2°C and 8°C.

Target Details for PROCR

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

Alternative Name: CD201

Background: 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.