Recombinant Human DDR1 Kinase / MCK10 / CD167 Protein (Catalog#10730-H08H)
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human DDR1 Kinase / MCK10 / CD167 (rh DDR1 Kinase / MCK10 / CD167; Catalog#10730-H08H; NP_001945.3; Met1-Thr416) and conjugated with APC under optimum conditions, the unreacted APC was removed.
Monoclonal Mouse IgG1 Clone #05
Aqueous solution containing 0.5% BSA and 0.09% sodium azide
5 μl/Test, 0.1 mg/ml
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. Protected from prolonged exposure to light. Do not freeze ! Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Flow cytometric analysis of Human DDR1(CD167a) expression on MCF-7 cells. Cells were stained with APC-conjugated anti-Human DDR1(CD167a). The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
Discoidin domain receptor family, member 1 (DDR1), also known as or CD167a (cluster of differentiation 167a), and Mammary carcinoma kinase 1 (MCK1), belongs to a subfamily of tyrosine kinase receptors with an extracellular domain homologous to Dictyostellium discoideum protein discoidin 1. Receptor tyrosine kinases play a key role in the communication of cells with their microenvironment. These kinases are involved in the regulation of cell growth, differentiation and metabolism. Expression of DDR1/MCK1/CD167 is restricted to epithelial cells, particularly in the kidney, lung, gastrointestinal tract, and brain. In addition, it has been shown to be significantly overexpressed in several human tumors. DDR1/MCK1/CD167 plays an important role in regulating attachment to collagen, chemotaxis, proliferation, and MMP production in smooth muscle cells. DDR1 functions in a feedforward loop to increase p53 levels and at least some of its effectors. Inhibition of DDR1 function resulted in strikingly increased apoptosis of wild-type p53-containing cells in response to genotoxic stress through a caspase-dependent pathway.