| Product name: |
Recombinant Human LAP (TGF-beta 1) |
| Description: |
Recombinant Human Transforming Growth Factor beta 1 is produced by our Mammalian expression system and the target gene encoding Leu30-Arg278(Cys33Ser) is expressed. |
| Accession: |
P01137 |
| Molecular weight: |
28.5 KDa |
| Apparent molecular weight: |
20-30 KDa, reducing conditions |
| Purity: |
Greater than 95% as determined by reducing SDS-PAGE. |
| Endotoxin: |
Less than 0.1 ng/µg (1 EU/µg) as determined by LAL test. |
| Redissolve: |
Always centrifuge tubes before opening.Do not mix by vortex or pipetting.
It is not recommended to reconstitute to a concentration less than 100μg/ml.
Dissolve the lyophilized protein in distilled water.
Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
| Storage: |
Lyophilized protein should be stored at < -20°C, though stable at room temperature for 3 weeks.
Reconstituted protein solution can be stored at 4-7°C for 2-7 days.
Aliquots of reconstituted samples are stable at < -20°C for 3 months. |
| Delivery condition: |
The product is shipped at ambient temperature.
Upon receipt, store it immediately at the temperature listed below. |
| 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. |
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