TGF-β/SMAD signalling
TGF-β / SMAD signalling. Latent TGF-β is activated by integrins, then binds TβRII, which recruits and phosphorylates TβRI (ALK5). Via SARA, TβRI phosphorylates SMAD2/3, which partner SMAD4 and enter the nucleus to run four programmes — EMT, fibrosis, cytostasis and immunosuppression (Treg / FOXP3). Non-canonical TAK1/p38 and PI3K/AKT arms add to this, and the pathway is braked by SMAD7 / SMURF2 and BAMBI. Click any protein for the matching Assay Genie In Vivo antibody or ELISA kit.
Activation & receptors. TGF-β is secreted latent, wrapped in its LAP/LTBP shell; integrins (e.g. αvβ6) and proteases release the active dimer. It is presented by the co-receptor betaglycan (TβRIII) to TβRII, a constitutive kinase that trans-phosphorylates TβRI (ALK5). The pseudoreceptor BAMBI competes to blunt this.
Canonical SMAD cascade. SARA presents the receptor-SMADs SMAD2 and SMAD3 for phosphorylation; they release, partner the co-SMAD SMAD4, and translocate to the nucleus to bind SMAD elements. The inhibitory SMAD7 and the E3 ligase SMURF2 form a negative-feedback loop that ubiquitinates and degrades the receptor. In parallel, TβRI activates TRAF6 → TAK1 → p38/JNK and PI3K → AKT (non-canonical).
Four programmes. The SMAD complex, with lineage cofactors, drives: EMT — SNAIL/ZEB1 repress E-cadherin and induce vimentin; fibrosis — α-SMA, collagen I, CTGF, PAI-1; cytostasis — p21; and potent immunosuppression — induction of FOXP3+ Tregs and suppression of cytotoxic T and NK cells. That last programme is why TGF-β is a leading immuno-oncology target: Assay Genie’s In Vivo functional-grade anti-TGF-β (1,2,3) blocks it, while every receptor, SMAD, kinase and target gene is covered by an ELISA kit. For research use only; not for diagnostic or therapeutic procedures. Mouse targets shown where available.
Every protein node links to a product: In Vivo anti-TGF-β for the ligand; the receptors, SMADs, kinases, EMT/fibrosis/cytostasis effectors and FOXP3 open the matching ELISA kit or antibody.