TGF beta 2/TGFB2 Protein, Mouse/Rat (HEK293)

In mammals, three different isoforms of TGF-β are described (TGF-β1, TGF-β2 and TGF-β3; transforming growth factor beta) to regulate apoptosis, proliferation, differentiation, migration and invasion processes utilising overlapping but not redundant mechanisms. All three isoforms are expressed in the liver, but their expression is differentially distributed among liver cell types. TGF-β2 expression in different liver cell types and is also associated with developmental defects and fibrotic diseases in mice^[1][2][3].
The sequence of amino acids in TGF-β2 proteins from different species is very stable, which leads to the conclusion that in the process of evolution, TGF-β2 has been only slightly altered, and that both in humans and in animals, its function is similar.
TGFβ2 is a transforming growth factor beta (TGFB) family cytokine, with members of this cytokine family playing broad regulatory roles and controlling key physiological processes including cell migration, proliferation and differentiation via signalling through type I and type II receptors (TGFβR1 and TGFβR2), with signals propagating via the downstream regulatory SMAD proteins. This TGFβ/SMAD pathway is frequently dysregulated in human cancer. TGFβ cytokines are capable of suppressing T cell growth in response to IL‐2. The degree of TGFβ2 expression correlated with the expression of several different markers of immune cell subsets within tumours. In addition, TGF-β2 regulates embryonic development and, therefore not surprisingly, global Tgfb2 null mice exhibit a wide range of developmental defects and perinatal mortality^[1][2][3].
TGF-β2 is an immune suppressor involved in the development of immune tolerance, and recombinant TGF-β2 incubation is more potent than TGF-β1 or TGF-β3 in suppressing macrophage inflammatory responses. TGF-β2 is shown to correlate with bad prognosis in intrahepatic CCAs and hepatocellular carcinoma. Mechanistically, canonical Smad signalling as well as crosstalk with Yap, Hippo, Wnt and β-catenin signalling have been demonstrated in the liver and other organs^[1][2][3].

Recombinant human TGF-β2 (0.125 ng/mL, 1 ng/mL, 4 ng/mL) induces nonpermissive culture podocytes switch to G2/M arrest and apoptosis, selectively at advanced TGF-β concentrations and specifically in association with suppression of Cdkn2b and activation of proapoptotic p38 mitogen-activated protein kinase, in conditionally immortalized murine podocytes^[4].
Recombinant TGF-β2 (0.25-2.5 ng/mL; for 72 h) shows a dose-dependent proliferation inhibition in rat epithelial cell line (IEC-6)^[6].

Recombinant mouse TGF-β2 (12 ng/kg; for 13 days; osmotic pump) treatment reverses the detrimental metabolic effects of high fat feeding in mice, reduces fat mass and attenuates white adipose tissue inflammation^[1].
Recombinant human TGF-β2 (20, 100, and 400 μg/kg; for 9 weeks) causes modest increases in systolic blood pressure and proteinuria and minimal tubular interstitial fibrosis in normal male Sprague Dawley rats^[5].