|Tested species reactivity||Human|
|Published species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide corresponding to a region within amino acids 1 and 76 of Human CCR6|
|Purification||Antigen affinity chromatography|
|Storage buffer||0.1M tris glycine, pH 7, with 10% glycerol|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:100-1:1000|
|Western Blot (WB)||1:500-1:3000|
* 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.
|Miscellaneous PubMed (MISC)||See 1 publications below|
PA5-29015 targets CCR6 in IHC (P) and WB applications and shows reactivity with Human samples.
The PA5-29015 immunogen is synthetic peptide corresponding to a region within amino acids 1 and 76 of Human CCR6.
This gene encodes a member of the beta chemokine receptor family, which is predicted to be a seven transmembrane protein similar to G protein-coupled receptors. The gene is preferentially expressed by immature dendritic cells and memory T cells. The ligand of this receptor is macrophage inflammatory protein 3 alpha (MIP-3 alpha). This receptor has been shown to be important for B-lineage maturation and antigen-driven B-cell differentiation, and it may regulate the migration and recruitment of dentritic and T cells during inflammatory and immunological responses. Alternatively spliced transcript variants that encode the same protein have been described for this gene.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Expression of CCL20 and Its Corresponding Receptor CCR6 Is Enhanced in Active Inflammatory Bowel Disease, and TLR3 Mediates CCL20 Expression in Colonic Epithelial Cells.
PA5-29015 was used in immunohistochemistry - paraffin section to assess the role of TLR3 in enterocytic CCL20 signaling
|Skovdahl HK,Granlund Av,Østvik AE,Bruland T,Bakke I,Torp SH,Damås JK,Sandvik AK||PloS one (10:null)||2015|