anti-human CD9 APC-conjugated, Clone MEM-61
Description
CD9 belongs to proteins of tetraspanin family that orchestrate cholesterol-associated tetraspanin- enriched signaling microdomains within the plasma membrane, forming complexes with each other as well as with integrins, membrane-anchored growth factors and other proteins. CD9 is involved in cell motility, osteoclastogenesis, neurite outgrowth, myotube formation, and sperm-egg fusion, plays roles in cell attachment and proliferation and is necessary for association of heterologous MHC II molecules on the dendritic cell plasma membrane which is important for effective T cell stimulation. CD9 is also considered as metastasis suppressor in solid tumors.
Properties
The monoclonal antibody ADG5005/L (clone MEM-16) is a murine monoclonal antibody, subclass IgG1 recognizing human CD9. The antibody has been purified from cell culture supernatant using Protein A affinity chromatography.
The purified antibody is conjugated with cross-linked Allophycocyanin (APC) under optimum conditions. The reagent is adjusted for direct use. No reconstitution is necessary.
Specificity
The antibody recognizes an epitope on second extracellular domain (EC2) of CD9 antigen, a 24 kDa single transmembrane polypeptide expressed on platelets, monocytes, pre-B lymphocytes, granulocytes and activated T lymphocytes.
HLDA VI; WS Code P P-15.
Presentation
Vial containing 500 µl (ADG5005) or 2 ml (ADG5005L) of purified antibody in PBS containing 1% BSA and 0.09% sodium azide (pH 7.2). Spin the vial briefly before opening.
Storage and Stability
Store the antibody at 4°C. Avoid prolonged exposure to light. The reagent is stable until the expiry date stated on the vial label.
Applications
Flow cytometry
Category: Research use only
Type: Antibody
Product Availability: Worldwide
Manufacturer: ImmBioMed GmbH & Co KG, Germany
For more information please click .pdf icon below.
anti-human CD9 APC-conjugated, Clone MEM-61
Cat.No. ADG5005
Article no.: 938012
Unit: 500 µl
Code: ADG5005
Manufacturer: ImmBioMed GmbH & Co. KG
References
- Haematologica. 2015 Jun;100(6):757-67. doi: 10.3324/haematol.2014.118497. Epub 2015 Apr 3.
Tetraspanin CD9 participates in dysmegakaryopoiesis and stromal interactions in primary myelofibrosis.
Desterke C, Martinaud C, Guerton B, Pieri L, Bogani C, Clay D, Torossian F, Lataillade JJ, Hasselbach HC, Gisslinger H, Demory JL, Dupriez B, Boucheix C, Rubinstein E, Amsellem S, Vannucchi AM, Le Bousse-Kerdilès MC.
The authors analyzed whether CD9 participates in the dysmegakaryopoiesis observed in patients with primary myelofibrosis. They asked, whether CD 9 is involved in the altered interplay between megakaryocytes and stromal cells. Their results indicate that CD9 plays a role in the dysmegakaryopoiesis that occurs in primary myelofibrosis and affects interactions between megakaryocytes and bone marrow stromal cells.
- Thromb Res. 1999 Sep 1;95(5):215-27.
Studies on the dual effects on platelets of a monoclonal antibody to CD9, and on the properties of platelet CD9.
Inngjerdingen M, Waterhouse K, Solum NO.
The authors found that binding of anti CD9 antibody to platelets exerts a dual action on human platelets in plasma depending on whether the complement system can be activated or not, resulting either in membrane permeabilization or a true platelet aggregation. Moreover, CD9 was found to be present on the surface of microvesicles derived from calcium ionophore-treated platelets.
- Br J Haematol. 1997 Feb;96(2):275-86.
Analysis of CD9, CD32 and p67 signalling: use of degranulated platelets indicates direct involvement of CD9 and p67 in integrin activation.
Slupsky JR, Cawley JC, Kaplan C, Zuzel M.
The authors found that, like intact cells, degranulated platelets can be activated and induced to aggregate by monoclonal antibodies against a 67 kD membrane protein (also known as PTA1) and CD9, and by crosslinked CD32 (Fcgamma-RII). They take their findings to suggest that the function of both CD9 and PTA1 antigen is closely associated with gpIIb/IIIa activation.
- Leukocyte Typing VI. Kishimoto T. et al. (Eds.), Garland Publishing Inc. (1997).