Anti-DDR2 Antibody Picoband® Fluoro488 Conjugated

Discoidin domain-containing receptor 2, also known as CD167b (cluster of differentiation 167b), is a protein that in humans is encoded by the DDR2 gene. This gene encodes a member of the discoidin domain receptor subclass of the receptor tyrosine kinase (RTKs) protein family. RTKs play a key role in the communication of cells with their microenvironment. The encoded protein is a collagen-induced receptor that activates signal transduction pathways involved in cell adhesion, proliferation, and extracellular matrix remodeling. This protein is expressed in numerous cell types and may alos be involved in wound repair and regulate tumor growth and invasiveness. Mutations in this gene are the cause of short limb-hand type spondylometaepiphyseal dysplasia.

Discoidin domain-containing receptor 2; Discoidin domain receptor 2; CD167 antigen-like family member B; Discoidin domain-containing receptor tyrosine kinase 2; Neurotrophic tyrosine kinase, receptor-related 3; Receptor protein-tyrosine kinase TKT; Tyrosine-protein kinase TYRO10; CD167b; DDR2; NTRKR3; TKT; TYRO10

Detected in osteocytes, osteoblastic cells in subchondral bone, bone lining cells, tibia and cartilage (at protein level) . Detected at high levels in heart and lung, and at low levels in brain, placenta, liver, skeletal muscle, pancreas, and kidney.

Tyrosine kinase that functions as cell surface receptor for fibrillar collagen and regulates cell differentiation, remodeling of the extracellular matrix, cell migration and cell proliferation. Required for normal bone development. Regulates osteoblast differentiation and chondrocyte maturation via a signaling pathway that involves MAP kinases and leads to the activation of the transcription factor RUNX2. Regulates remodeling of the extracellular matrix by up-regulation of the collagenases MMP1, MMP2 and MMP13, and thereby facilitates cell migration and tumor cell invasion. Promotes fibroblast migration and proliferation, and thereby contributes to cutaneous wound healing.

1. Bargal, R., Cormier-Daire, V., Ben-Neriah, Z., Le Merrer, M., Sosna, J., Melki, J., Zangen, D. H., Smithson, S. F., Borochowitz, Z., Belostotsky, R., Raas-Rothschild, A.Mutations in DDR2 gene cause SMED with short limbs and abnormal calcifications. Am. J. Hum. Genet. 84: 80-84, 2009. 2. Borochowitz, Z., Langer, L. O., Jr., Gruber, H. E., Lachman, R., Katznelson, M. B.-M., Rimoin, D. L.Spondylo-meta-epiphyseal dysplasia (SMED), short limb-hand type: a congenital familial skeletal dysplasia with distinctive features and histopathology. Am. J. Med. Genet. 45: 320-326, 1993. 3. Labrador, J. P., Azcoitia, V., Tuckermann, J., Lin, C., Olaso, E., Manes, S., Bruckner, K., Goergen, J.-L., Lemke, G., Yancopoulos, G., Angel, P., Martinez-A, C., Klein, R.The collagen receptor DDR2 regulates proliferation and its elimination leads to dwarfism. EMBO J. 2: 446-452, 2001.