Recombinant human ROR2 Protein with C-6×His tag
Figure 1. Human ROR2 Protein, His Tag on SDS-PAGE under reducing condition.
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| Amount : | 50 µg |
| Purification : | The purity of the protein is greater than 95% as determined by SDS-PAGE and Coomassie blue staining. |
| Content : | Lyophilized from sterile PBS, pH 7.4. Normally 5 % - 8 % trehalose is added as protectants before lyophilization. |
| Storage condition : | Store at -80°C for 12 months (Avoid repeated freezing and thawing) |
| Alternative Name : | ROR2,NTRKR2 |
Expression Host : HEK293
The protein has a predicted molecular mass of 42.2 kDa after removal of the signal peptide.The apparent molecular mass of ROR2-His is approximately 55-70 kDa due to glycosylation.
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.
The protein has a predicted molecular mass of 42.2 kDa after removal of the signal peptide.The apparent molecular mass of ROR2-His is approximately 55-70 kDa due to glycosylation.
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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