Recombinant Mouse ROR2 mFc Chimera Protein, CF Summary
Product Specifications
Mouse ROR2 (Glu34-Gly403) Accession # NP_038874.3 | IEGRMDP | Mouse IgG2A (Glu98-Lys330) |
N-terminus | C-terminus | |
Analysis
Product Datasheets
Carrier Free
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
11425-RO
Formulation | Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. See Certificate of Analysis for details. |
Reconstitution | Reconstitute at 500 μg/mL in PBS. |
Shipping | The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. |
Stability & Storage: | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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Scientific Data
Recombinant Mouse ROR2 mFc Chimera Protein (Catalog # 11425-RO) binds Human ROR2 Antibody (AF2064) with an ED50 of 0.600‑7.20 ng/mL.
2 μg/lane of Recombinant Mouse ROR2 mFc Chimera Protein (Catalog # 11425-RO) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing bands at 80-88 kDa and 160-180 kDa, respectively.
Reconstitution Calculator
Background: ROR2
ROR2 (Receptor Tyrosine Kinase-like Orphan Receptor 2) is a member of the ROR family of receptor tyrosine kinases and is important for skeletal development, including bone and cartilage formation, as well as for the development of the central nervous system (1-5). Mature mouse ROR2 contains a 370 amino acid (aa) extracellular domain (ECD) and a 520 aa cytoplasmic tail containing an tyrosine kinase domain. The ROR2 ECD features an immunoglobulin domain, a cysteine-rich domain that resembles the Wnt-binding sites of Frizzled proteins, and a kringle domain. The ECD of mouse ROR2 shares 94% and 99% aa sequence identity with the ECD of human and rat ROR2, respectively. ROR2 binds the Wnt family ligand, Wnt-5a, to activate non-canonical Wnt signaling pathways (6-8). ROR2 is broadly expressed during embryonic development and can be found in cells of all three germ layers as well as in most organ tissues (9, 10). Activation of ROR2 signaling promotes cellular proliferation, differentiation, cell-polarization, and migration. ROR2 is important for osteogenic and chondrogenic differentiation of mesenchymal stem cells (11, 12). Mutations in ROR2 are associated with the skeletal disorders, brachydactyly type B and Robinow syndrome (6). ROR2 is also involved in neurite outgrowth and synapse development in the brain (4). A variety of tumors have been found to over-express ROR2. Depending upon the cellular context, ROR2 can act as a tumor suppressor or promoter (13). Expression of ROR2 within carcinomas is correlated with a poor prognosis of survival and increased rates of recurrence (14-16).
- DeChiara, T.M. et al. (2000) Nat. Genet. 24:271.
- Petrova, I.M. et al. (2014) Mol. Neurobiol. 49:303.
- Takeuchi, S. et al. (2000) Genes Cells 5:71.
- Paganoni, S. and A. Ferreira (2003) J. Neurosci. Res. 73:429.
- Endo, M. et al. (2012) J. Cell. Sci. 125:2017.
- Minami, Y. et al. (2010) Dev. Dyn. 239:1.
- Oishi, I. et al. (2003) Genes Cells 8:645.
- Wallkamm, V. et al. (2014) PLoS ONE 9:e109428.
- Al-Shawi, R. et al. (2001) Dev. Genes. Evol. 211:161.
- Matsuda, T. et al. (2001) Mech. Dev. 105:153.
- Cai, S.X. et al. (2014) J. Cell. Physiol. 229:791.
- Xin, H. et al. (2013) Int. J. Mol. Med. 31:583.
- Ford, C.E. et al. (2013) Int. J. Cancer 133:779.
- Rasmussen, N.R. et al. (2014) PLoS ONE 9:e116101.
- Mei, H. et al. (2014) Biochem. Biophys. Res. Commun. 453:703.
- Lu, B.J. et al. (2012) Mol. Med. Rep. 5:1033.
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