LRRC32 anticorps

N° du produit ABIN2664991

L’anticorps Rat Monoclonal anti-LRRC32 a été validé pour IHC, CyTOF et ELISA (Capture). Il convient pour détecter LRRC32 dans des échantillons de Souris.

Aperçu rapide pour LRRC32 anticorps (ABIN2664991)

Antigène: LRRC32 (Leucine Rich Repeat Containing 32 (LRRC32))

Reactivité: Souris

Hôte: Rat

Clonalité: Monoclonal

Conjugué: Cet anticorp LRRC32 est non-conjugé

Application: Immunohistochemistry (IHC), Cytometry by Time of Flight (CyTOF), ELISA (Capture)

Clone: F011-5

Détail du produit anti-LRRC32 anticorps

Purification: The antibody was purified by affinity chromatography.

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: 0.5 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 LRRC32

Antigène: LRRC32 (Leucine Rich Repeat Containing 32 (LRRC32))

Autre désignation: GARP

Sujet: Glycoprotein A Repetitions Predominant (GARP), also known as leucine rich repeat containing protein 32 (LRC32), is a 80 kD type I membrane glycoprotein with 20 leucine rich repeats in the extracellular portion of the protein. GARP was found on the surface of megakaryocytes, platelets, and activated Tregs. It serves as a receptor for latent TGF-β. Recent evidence suggests that GARP may play a role in controlling suppressor function of Tregs. A mutation in GARP has been reported in a large Samaritan kindred with Usher syndrome type 1. In addition, it has been found that GARP mRNA is highly amplified in different tumors, which indicates that tumor cells may use GARP to express TGF-β or to capture TGF-β from their surroundings, resulting in local suppression of anti-tumor immune responses or the induction of Tregs.

Pathways: Activated T Cell Proliferation