Human TGF-β2(Transforming Growth Factor Beta 2) ELISA Kit (E-EL-H1587)

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-β2. 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-β2 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-β2, 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-β2. You can calculate the concentration of Human TGF-β2 in the samples by comparing the OD of the samples to the standard curve.

Transforming growth factor beta-2 (TGF-beta 2) is a multifunctional secreted cytokine of the TGF-beta superfamily and one of three mammalian isoforms encoded by separate genes. It is synthesized as a proprotein that is cleaved into a latency-associated peptide and the mature TGF-beta 2 chain, persists as an inactive latent complex bound to the extracellular matrix until activated by integrins, proteases or thrombospondin-1, and shares the characteristic dimeric cysteine-knot architecture of TGF-beta family ligands. Like TGF-beta 1 and TGF-beta 3, TGF-beta 2 signals through heteromeric TGFBR1/TGFBR2 receptor complexes that phosphorylate Smad2 and Smad3 and, together with Smad4, drive target-gene transcription alongside non-Smad pathways. It regulates proliferation, differentiation, apoptosis, extracellular matrix production and tissue morphogenesis, is indispensable for angiogenesis and cardiac development, and can either suppress or promote growth depending on the cellular context. Aberrant TGF-beta 2 signaling contributes to fibrosis, cancer and developmental defects. Elevated expression is associated with excessive matrix deposition in fibrotic disorders and with immune suppression, epithelial-mesenchymal transition and invasion in the tumor microenvironment, and quantitative detection of TGF-beta 2 supports research on embryonic development, fibrogenesis, ocular and cardiac disease, cancer biology and therapies that modulate TGF-beta family activity.