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Antigenic Specificity | CD167a (DDR1), Human |
Clone | 51D6 |
Host Species | Mouse |
Reactive Species | human |
Isotype | IgG3κ |
Format | biotin conjugate |
Size | 100 tests in 1 mL |
Concentration | 1:11 |
Applications | Mass cytometry |
Reviews / Ratings | If you have used this antibody, please help fellow researchers by submitting reviews to pAbmAbs and antYbuddY. |
Description | CD167a (DDR1) Antibody, anti-human, Biotin. Clone 51D6 recognizes the human CD167a antigen, a single-pass type I membrane protein, which is also known as discoidin domain receptor (DDR1), mammary carcinoma kinase 10 (MCK-10), or tyrosine kinase receptor E (trkE). CD167a is a tyrosine kinase that functions as cell surface receptor for fibrillar collagen and regulates cell attachment to the extracellular matrix, remodeling of the extracellular matrix, cell migration, differentiation, survival, and cell proliferation. It promotes smooth muscle cell migration, and thereby contributes to arterial wound healing. CD167a also plays a role in tumor cell invasion. Three isoforms of CD167a have been reported. CD167a is expressed on epithelial cells, keratinocytes, leukocytes, monocytes, and has been reported to be overexpressed in some breast carcinomas. | |
Immunogen | n/a |
Other Names | HGK2, MCK-10, RTK-6, TRK E, DDR, CAK |
Gene, Accession # | Gene ID: 780 |
Catalog # | 130-110-088 |
Price | $264 |
Order / More Info | CD167a (DDR1), Human Antibody from MILTENYI BIOTEC B.V. & Co. KG |
Product Specific References | Di Marco, E. et al. (1993) Molecular cloning of trkE, a novel trk-related putative tyrosine kinase receptor isolated from normal human keratinocytes and widely expressed by normal human tissues. J. Biol. Chem. 268 (32): 2490-2495. | Canning, P. et al. (2014) Structural mechanisms determining inhibition of the collagen receptor DDR1 by selective and multi-targeted type II kinase inhibitors. J. Mol. Biol. 426 (13): 2457-2470. | Hohenester, E. (2014) Signalling complexes at the cell-matrix interface. Curr. Opin. Struct. Biol. 29C: 10-16. |