|Other Names||Tyrosine-protein kinase transmembrane receptor ROR2, Neurotrophic tyrosine kinase, receptor-related 2, ROR2, NTRKR2|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP7672a was selected from the N-term region of human ROR2 . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Tyrosine-protein kinase receptor which may be involved in the early formation of the chondrocytes. It seems to be required for cartilage and growth plate development (By similarity). Phosphorylates YWHAB, leading to induction of osteogenesis and bone formation (PubMed:17717073). In contrast, has also been shown to have very little tyrosine kinase activity in vitro. May act as a receptor for wnt ligand WNT5A which may result in the inhibition of WNT3A-mediated signaling (PubMed:25029443).|
|Cellular Location||Cell membrane; Single-pass type I membrane protein|
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ROR2 is a tyrosine-protein kinase receptor which may be involved in the early formation of the chondrocytes. It seems to be required for cartilage and growth plate development. This Type I membrane protein is expressed at high levels during early embryonic development. The expression levels drop strongly around day 16 and there are only very low levels in adult tissues. Defects in ROR2 are a cause of brachydactyly type B1 (BDB1). BDB1 is an autosomal dominant skeletal disorder characterized by hypoplasia/aplasia of distal phalanges and nails. In BDB1 the middle phalanges are short but in addition the terminal phalanges are rudimentary or absent. Both fingers and toes are affected. The thumbs and big toes are usually deformed. Defects in ROR2 are a cause of recessive Robinow syndrome (RRS). RRS is an autosomal disorder characterized by skeletal dysplasia with generalized limb bone shortening, segmental defects of the spine, brachydactyly and a dysmorphic facial appearance. The protein contains 1 frizzled (FZ) domain, 1 immunoglobulin-like C2-type domain, and 1 kringle domain.
Afzal, A.R., et al., Nat. Genet. 25(4):419-422 (2000).Oldridge, M., et al., Nat. Genet. 24(3):275-278 (2000).van Bokhoven, H., et al., Nat. Genet. 25(4):423-426 (2000).Schwabe, G.C., et al., Am. J. Hum. Genet. 67(4):822-831 (2000).Masiakowski, P., et al., J. Biol. Chem. 267(36):26181-26190 (1992).
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