Immunofluorescent analysis of CD106 (green) showing staining in the cytoplasm of HUVEC cells treated with human TNF-alpha (right) compared to untreated HUVEC cells (left). Formalin-fixed cells were permeabilized with 0.1% Triton X-100 in TBS for 5-10 minutes and blocked with 3% BSA-PBS for 30 minutes at room temperature. Cells were probed with a CD106 monoclonal antibody (Product # MA5-11447) in 3% BSA-PBS at a dilution of 1:20 and incubated overnight at 4 °C in a humidified chamber. Cells were washed with PBST and incubated with a DyLight-conjugated secondary antibody in PBS at room temperature in the dark. F-actin (red) was stained with a flourescent red phalloidin and nuclei (blue) were stained with Hoechst or DAPI. Images were taken at a magnification of 60x.
|Tested species reactivity||Human, Mouse|
|Published species reactivity||Rat, Human|
|Host / Isotype||Mouse / IgG1|
|Immunogen||Stimulated human umbilical vein endothelial cells (HUVEC)|
|Storage buffer||PBS, pH 7.4, with 0.2% BSA|
|Contains||0.09% sodium azide|
|Storage Conditions||4° C|
|Tested Applications||Dilution *|
|Immunohistochemistry (Frozen) (IHC (F))||1:12.5-1:25|
|Immunohistochemistry (Paraffin) (IHC (P))||1:12.5-1:25|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
MA5-11447 targets CD106 in IHC (P, F) and ICC/IF applications and shows reactivity with Human samples.
The MA5-11447 immunogen is stimulated human umbilical vein endothelial cells (HUVEC).
MA5-11447 has been successfully used in immunohistochemistry analysis of VCAM1 in mouse E16.5 frozen lung sections.
CD106 (also known as vascular cell adhesion molecule-1 (VCAM-1) and INCAM-110) is a member of the Ig superfamily of adhesion molecules and is expressed at high levels on cytokine stimulated vascular endothelial cells, and at minimal levels on unstimulated endothelial cells. It is also present on follicular and interfollicular dendritic cells of lymph nodes, myoblasts, and some macrophages. CD106 serves as a ligand for leukocyte integrin alphaBeta (VLA-4 or CD49d/CD29) and mediates cell adhesion of leukocytes to activated endothelium. It plays a role in tumor metastasis.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Inhibition of cell surface expression of endothelial adhesion molecules by ursolic acid prevents intimal hyperplasia of venous bypass grafts in rats.
MA5-11447 was used in immunohistochemistry to study the role of reduced endothelial VCAM-1 expresson in the mechanism by which ursolic acid prevents intimal hyperplasia in a rat model of venous bypass graft
|Zeller I,Wiedemann D,Schwaiger S,Stelzmüller M,Kreutmayer S,Leberfing O,Stuppner H,Bernhard D||European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery (42:878)||2012|
Immunophenotypic profile and role of adhesion molecules in splenic marginal zone lymphoma with bone marrow involvement.
MA5-11447 was used in immunohistochemistry to study the distribution and function of adhesion molecules in splenic marginal zone lymphoma
|Florena AM,Tripodo C,Porcasi R,Ingrao S,Fadda MR,De Cantis S,Iannitto E,Franco V||Leukemia and lymphoma (47:49)||2006|
Identification and pharmacological characterization of the anti-inflammatory principal of the leaves of dwarf elder (Sambucus ebulus L.).
MA5-11447 was used in immunocytochemistry to identify and study the active anti-inflammatory component of dwarf elder leaves
|Schwaiger S,Zeller I,Pölzelbauer P,Frotschnig S,Laufer G,Messner B,Pieri V,Stuppner H,Bernhard D||Journal of ethnopharmacology (133:704)||2011|
Leoligin, the major lignan from Edelweiss, inhibits intimal hyperplasia of venous bypass grafts.
MA5-11447 was used in flow cytometry to study the mechanism by which leoligin inhibits intimal hyperplasia of venous bypass grafts
|Reisinger U,Schwaiger S,Zeller I,Messner B,Stigler R,Wiedemann D,Mayr T,Seger C,Schachner T,Dirsch VM,Vollmar AM,Bonatti JO,Stuppner H,Laufer G,Bernhard D||Cardiovascular research (82:542)||2009|