Human TGF-β3(Transforming Growth Factor Beta 3) ELISA Kit (E-EL-H2339)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Human TGF-β3. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Human TGF-β3 and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Human TGF-β3, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Human TGF-β3. You can calculate the concentration of Human TGF-β3 in the samples by comparing the OD of the samples to the standard curve.

Transforming growth factor beta-3 (TGF-beta 3) is a secreted cytokine of the TGF-beta superfamily and one of three mammalian isoforms that share the characteristic dimeric cysteine-knot fold. It is synthesized as a proprotein cleaved into a latency-associated peptide and the mature chain, secreted as a latent complex sequestered in the extracellular matrix, and subsequently activated by integrins, proteases, thrombospondin-1 or mechanical traction that release the active ligand. TGF-beta 3 signals through heteromeric TGFBR1/TGFBR2 receptor complexes to phosphorylate Smad2 and Smad3, which together with Smad4 regulate transcription of genes controlling cell proliferation, differentiation, extracellular matrix production, epithelial-mesenchymal transition, wound contraction and immune suppression. It differs from TGF-beta 1 and TGF-beta 2 in receptor affinity, potency and developmental expression, and in wound healing it limits fibroblast recruitment, myofibroblast differentiation and collagen deposition, exerting a stronger anti-fibrotic effect than TGF-beta 1 and contributing to the scarless healing of fetal skin and oral mucosa. Dysregulated TGF-beta 3 is implicated in tissue fibrosis, tumor progression and developmental defects including cleft palate and abnormal lung and heart morphogenesis, and recombinant TGF-beta 3 has been evaluated clinically for wound healing, scar reduction and oral mucositis. Measurement of TGF-beta 3 supports research on wound repair, fibrosis, palate and lung development and developmental biology, and quantification of the cytokine is useful for assessing fibrotic activity in tissue repair and scar regulation.