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ManualCOAMSDSTGFβ-1, a secreted TGF-β superfamily protein, is abundant in bone, cartilage and chondrocytes and elevated in OA. It controls cell proliferation, differentiation and apoptosis. Its precursor is cleaved to yield LAP and mature TGFβ-1, and can form heterodimers with other TGF-β proteins. Tumors often overexpress TGFβ-1; TGFB1 mutations cause Camurati-Engelmann disease.
| Synonyms | TGF-β1, DPD1, IBDIMDE, LAP, TGF-beta1, TGFB, TGFB1 |
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| Protein Construction ＆ Source | •(Uniprot: P01137) Recombinant Human TGF-β1 Protein is expressed from HEK293 cells with His tag at the C-terminus. It contains AA Met1-Ser390. •The protein has a predicted MW of 44.6 kDa. Under reducing(R) SDS-PAGE conditions, the protein shows bands at 15, 45 and 55 kDa due to glycosylation, corresponding to mature TGFβ1, LAP and inactive latent TGFβ1 monomer, respectively. In non-reduced SDS-PAGE, it migrates at approximately 110 kDa, representing a complex of TGFβ1 homodimer non-covalently associated with a LAP homodimer. |
| Endotoxin | < 0.1 EU per ug as determined by the LAL method. |
| Purity | > 90% as determined by SDS-PAGE. |
| Concentration ＆ Formulation | •1.81 mg/mL•Filtered through a 0.22 μm filter, stored in 1x PBS, pH 7.4. |
| Target background | TGFβ-1, a secreted TGF-β superfamily protein, is abundant in bone, cartilage and chondrocytes and elevated in OA. It controls cell proliferation, differentiation and apoptosis. Its precursor is cleaved to yield LAP and mature TGFβ-1, and can form heterodimers with other TGF-β proteins. Tumors often overexpress TGFβ-1; TGFB1 mutations cause Camurati-Engelmann disease. |
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