Product Description
ROR2 Antibody | 63-131 | ProSci
Host: Rabbit
Reactivity: Human
Homology: N/A
Immunogen: This ROR2 antibody is generated from rabbits immunized with a recombinant protein of human ROR2.
Research Area: Signal Transduction
Tested Application: WB, IHC-P
Application: For WB starting dilution is: 1:1000
For IHC-P starting dilution is: 1:10~50
Specificiy: N/A
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: 105 kDa
Validation: N/A
Isoform: N/A
Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis
Clonality: Polyclonal
Clone: N/A
Isotype: Rabbit Ig
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.
Concentration: batch dependent
Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Alternate Name: Tyrosine-protein kinase transmembrane receptor ROR2, Neurotrophic tyrosine kinase, receptor-related 2, ROR2, NTRKR2
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: 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.