TGF-β/SMAD Signaling Pathway Research Reagents

TGF-β1 — The most abundant and extensively studied TGF-β isoform. TGF-β1 is a master regulator of fibrosis, immune suppression, and epithelial-mesenchymal transition (EMT). It is secreted as a latent complex and activated by integrins, thrombospondin-1, or proteolytic cleavage. Recombinant TGF-β1 is widely used in T_reg differentiation, fibrosis models, and EMT induction assays.
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TGF-β2 — Critical for cardiac development, palate fusion, and ocular physiology. Elevated TGF-β2 in the aqueous humor contributes to trabecular meshwork fibrosis in primary open-angle glaucoma.
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TGF-β3 — Plays a non-redundant role in palatal fusion and scarless wound healing. TGF-β3 promotes mesenchymal cell migration and is investigated as a therapeutic target for scar reduction.
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BMP-2 (Bone Morphogenetic Protein 2) — A potent inducer of osteoblast differentiation and bone formation via the SMAD1/5/9 branch. Recombinant BMP-2 is used in osteogenic differentiation assays, stem cell research, and skeletal tissue engineering models.
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TβRII (TGFBR2) — The type II receptor with constitutive kinase activity. Upon TGF-β ligand binding, TβRII recruits and trans-phosphorylates the type I receptor (ALK5), which in turn phosphorylates downstream R-SMADs. Frameshift mutations in TGFBR2 are frequently observed in microsatellite instability-high (MSI-H) colorectal cancers. Recombinant TβRII-Fc fusion proteins serve as ligand traps in TGF-β neutralization assays.
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ALK5 (TGFBR1) — The principal type I receptor for TGF-β1/2/3 signaling that directly phosphorylates SMAD2/3. ALK5 kinase inhibitors (e.g., SB431542, galunisertib) are widely used research tools and clinical candidates for fibrosis and oncology.
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Endoglin (CD105) — A TGF-β co-receptor highly expressed on proliferating endothelial cells. Endoglin is a validated marker for tumor angiogenesis and a target in anti-angiogenic therapy. Mutations in ENG cause hereditary hemorrhagic telangiectasia type 1 (HHT1).
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SMAD2/3 — Receptor-regulated SMADs (R-SMADs) that are directly phosphorylated by ALK4/5/7 upon TGF-β or Activin stimulation. Phospho-SMAD2/3 antibodies are essential readouts for pathway activation in Western blot, IHC, and flow cytometry.
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SMAD4 — The common-mediator SMAD (Co-SMAD) that partners with phosphorylated R-SMADs to form transcriptionally active complexes in the nucleus. SMAD4 is a tumor suppressor frequently inactivated in pancreatic ductal adenocarcinoma (PDAC) and colorectal cancer. Loss of SMAD4 expression by IHC is used as a prognostic biomarker.
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SMAD7 — An inhibitory SMAD (I-SMAD) that provides negative feedback by recruiting SMURF E3 ubiquitin ligases to degrade activated type I receptors. SMAD7 overexpression blocks TGF-β-induced fibrosis. In inflammatory bowel disease, elevated SMAD7 impairs mucosal TGF-β signaling; antisense oligonucleotide-mediated knockdown of SMAD7 (e.g., mongersen) has been explored as a therapeutic strategy to restore anti-inflammatory TGF-β activity.
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1. Massagué J. TGFβ signalling in context. Nat Rev Mol Cell Biol. 2012;13(10):616-630. DOI

2. Derynck R, Zhang YE. Smad-dependent and Smad-independent pathways in TGF-β family signalling. Nature. 2003;425(6958):577-584. DOI

3. Batlle E, Massagué J. Transforming growth factor-β signaling in immunity and cancer. Immunity. 2019;50(4):924-940. DOI

4. Hahn SA, et al. DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1. Science. 1996;271(5247):350-353. DOI