|Tested species reactivity||Human|
|Host / Isotype||Rabbit / IgG|
|Immunogen||KLH conjugated synthetic peptide between 19-50 amino acids from the N-terminal region of human ROR2|
|Purification||Ammonium sulfate precipitation, Size-exclusion - Dialysis|
|Contains||0.09% sodium azide|
|Storage Conditions||-20° C, Avoid Freeze/Thaw Cycles|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||1:10-1:50|
|Immunohistochemistry (Paraffin) (IHC (P))||1:10-1:50|
|Western Blot (WB)||1:1000|
* 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.
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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.