Recombinant Human LAP (TGF-beta 1)

Recombinant Human LAP (TGF-beta 1)

Size1:10μg price1:$89
Size2:50μg price2:$248
Size3:500μg price3:$2350
SKU: PHH2193 Category: Target Proteins Tags: ,

Datasheet

Name

Recombinant Human LAP (TGF-beta 1)

Purity

Greater than 95% as determined by reducing SDS-PAGE

Endotoxin level

<1 EU/µg as determined by LAL test.

Construction

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

Host

Human Cells

Species

Human

Predicted Molecular Mass

28.5 KDa

Buffer

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.

Form

Lyophilized

Shipping

The product is shipped at ambient temperature.Upon receipt, store it immediately at the temperature listed below.

Stability&Storage

Store at ≤-70°C, stable for 6 months after receipt.Store at ≤-70°C, stable for 3 months under sterile conditions after opening. Please minimize freeze-thaw cycles.

Reconstitution

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.

 

 

 

Alternative Names

Transforming Growth Factor Beta-1; TGF-Beta-1; Latency-Associated Peptide; LAP; TGFB1; TGFB

 

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.

 

Note

For Research Use Only , Not for Diagnostic Use.