Human ROR2(Tyrosine-protein kinase transmembrane receptor ROR2) ELISA Kit
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Product specifications
| Category | ELISA Kits |
| Reactivity | human |
| Detection Method | Colorimetric |
| Assay Data | Quantitative |
| Assay Type | Sandwich ELISA, Double Antibody |
| Test Range | 0.156-10ng/ml |
| Size 1 | 96T |
| Sample Type | Busacar en las instrucciones |
| Availability | Shipped within 10-14 working days. |
| Storage | 2-8 °C for 6 months |
| UniProt ID | Q01974 |
| Alias | BDB,BDB1,NTRKR2,Neurotrophic tyrosine kinase, receptor-related 2,Tyrosine-protein kinase transmembrane receptor ROR2 |
| Background | Elisa Kits ROR2 |
| Status | RUO |
ROR2 (Receptor Tyrosine Kinase-Like Orphan Receptor 2) is closely related to ROR1 but has distinct functions, particularly in skeletal and cardiovascular development. ROR2 acts as a coreceptor for Wnt5a in the planar cell polarity pathway, essential for cell movement and polarity during embryogenesis. Mutations in the ROR2 gene have been associated with Robinow syndrome and brachydactyly type B, which are developmental disorders affecting skeletal and facial structures. ROR2 is also implicated in cancer biology, where its expression correlates with aggressive tumor behaviors, including invasion and metastasis. Its dual roles in development and disease make ROR2 a critical player in both developmental biology and oncology research.
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ROR2 Antibody is a Rabbit Polyclonal antibody against ROR2. The protein encoded by this gene is a receptor protein tyrosine kinase and type I transmembrane protein that belongs to the ROR subfamily of cell surface receptors. The protein may be involved in the early formation of the chondrocytes and may be required for cartilage and growth plate development. Mutations in this gene can cause brachydactyly type B, a skeletal disorder characterized by hypoplasia/aplasia of distal phalanges and nails. In addition, mutations in this gene can cause the autosomal recessive form of Robinow syndrome, which is characterized by skeletal dysplasia with generalized limb bone shortening, segmental defects of the spine, brachydactyly, and a dysmorphic facial appearance.
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