Recombinant Human LAP (TGF-beta 1)
Recombinant Human Transforming Growth Factor beta 1 is produced by our Mammalian expression system and the target gene encoding Leu30-Arg278(Cys33Ser) is expressed.
Description
| Reference | ESCIT048 |
|---|---|
| Size | 10ug |
| Molecular Weight | 28.5 KDa |
| 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. |
| Biological Activity |
Other names: Transforming Growth Factor Beta-1; TGF-Beta-1; Latency-Associated PESCItide; LAP; TGFB1; TGFB
Redissolve: Always centrifuge tubes before opening.Do not mix by vortex or pipetting.
It is not recommended to reconstitute to a concentration less than 100?g/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.
Background: Transforming Growth Factor ?-1 (TGF?-1) is a secreted protein which belongs to the TGF-? family. TGF?-1 is abundantly expressed in bone, articular cartilage and chondrocytes and is increased in osteoarthritis (OA). TGF?-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 pESCItide (LAP) and a mature TGF?-1 pESCItide.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.