Recombinant Human TGF-β1

Description

EnkiLife provides the Recombinant Human TGF-β1 protein,aslo know as Transforming Growth Factor Beta-1, TGF-Beta-1, Latency-Associated Peptide, LAP, TGFB1, TGFB, which features high purity, high activity, and high stability. It can be applied in scientific research, biopharmaceuticals, and other fields.Purity:Greater than 95% as determined by reducing SDS-PAGE;Endotoxin Level:≤10 EU/mg;Construction:Recombinant Human TGF-β1 is produced by our Mammalian cell expression system and the target gene encoding Ala279-Ser390 is expressed.Accession:P01137. Expression Host:Human Cells.Species:Human.Predicted Molecular Mass:12.8 kDa. Background:Transforming Growth Factor β-1 (TGFβ-1) is a secreted protein which belongs to the TGF-β family. TGFβ-1 is abundantly expressed in bone, articular cartilage and chondrocytes and is increased in osteoarthritis (OA). TGFβ-1 performs many cellular functions, including the control of cell growth, cell proliferation, cell differentiation and apoptosis. The precursor is cleaved into a latency-associated peptide (LAP) and a mature TGFβ-1 peptide.Disulfide-linked homodimers of LAP and TGF-beta 1 remain non-covalently associated after secretion, forming the small latent TGF-beta 1 complex. Purified LAP is also capable of associating with active TGF-beta with high affinity, and can neutralize TGF-beta activity. Covalent linkage of LAP to one of three latent TGF-beta binding proteins (LTBPs) creates a large latent complex that may interact with the extracellular matrix. TGF-beta activation from latency is controlled both spatially and temporally, by multiple pathways that include actions of proteases such as plasmin and MMP9, and/or by thrombospondin 1 or selected integrins. Although different isoforms of TGF-beta are naturally associated with their own distinct LAPs, the TGF-beta 1 LAP is capable of complexing with, and inactivating, all other human TGF-beta isoforms and those of most other species. Mutations within the LAP are associated with Camurati-Engelmann disease, a rare sclerosing bone dysplasia characterized by inappropriate presence of active TGF-beta 1.