Smad3
SMAD3 is a receptor-regulated transcription factor in the TGF-β pathway, and activated TGF-β receptors phosphorylate SMAD3 to form SMAD complexes that regulate target-gene transcription[1]. Mechanistically, SMAD3 participates in cell proliferation, apoptosis, immune suppression, epithelial-mesenchymal transition, and extracellular matrix expression, making it useful for fibrosis, cancer progression, and inflammatory signaling studies[2][3]. In fibrosis models, SMAD3 acts as an important mediator of TGF-β profibrotic responses, and Smad3-deficient cells show reduced responses to selected chemotactic and matrix-related signals[3]. In cancer, SMAD3 can function as either a negative or positive regulator of carcinogenesis depending on cell type and tumor stage[2]. Compared with SMAD2, SMAD3 shows distinct regulation of TGF-β target genes and performs different functions in FOXH1-associated transcriptional control[4][5]. For experimental applications, SIS3 selectively inhibits TGF-β1-induced SMAD3 phosphorylation and SMAD3-SMAD4 interaction, making it a practical tool for testing SMAD3-dependent mechanisms[6].
References:
- [1]. Hata A, et al. TGF-β signaling from receptors to Smads. Cold Spring Harb Perspect Biol. 2016;8(9):a022061. [Content Brief]
- [2]. Millet C, et al. Roles of Smad3 in TGF-beta signaling during carcinogenesis. Crit Rev Eukaryot Gene Expr. 2007;17(4):281-293. [Content Brief]
- [3]. Flanders KC. Smad3 as a mediator of the fibrotic response. Int J Exp Pathol. 2004;85(2):47-64. [Content Brief]
- [4]. Brown KA, et al. A tale of two proteins: differential roles and regulation of Smad2 and Smad3 in TGF-beta signaling. J Cell Biochem. 2007;101(1):9-33. [Content Brief]
- [5]. Aragón E, et al. Structural basis for distinct roles of SMAD2 and SMAD3 in FOXH1 pioneer-directed TGF-β signaling. Genes Dev. 2019;33(21-22):1506-1524. [Content Brief]
- [6]. Jinnin M, et al. Characterization of SIS3, a novel specific inhibitor of Smad3, and its effect on transforming growth factor-beta1-induced extracellular matrix expression. Mol Pharmacol. 2006;69(2):597-607. [Content Brief]
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Smad3 Related Products (5)
Related Products (5)
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(S,R,S)-AHPC-C2-amide-benzofuranylmethyl-pyridine
0 Images(S,R,S)-AHPC-C2-amide-benzofuranylmethyl-pyridine is a dual-targeting PROTAC molecule. (S,R,S)-AHPC-C2-amide-benzofuranylmethyl-pyridine not only targets the ubiquitination and degradation of Smad3, but also elevates the protein level of HIF-α, thereby exerting multi-pathway anti-fibrotic and renoprotective effects. (S,R,S)-AHPC-C2-amide-benzofuranylmethyl-pyridine can be used in a wide range of tumor studies including cancers with KRAS inhibitor resistance, covering pancreatic ductal adenocarcinoma, acute myeloid leukemia, and various soft tissue sarcomas (such as fibrosarcoma, liposarcoma, chondrosarcoma, etc.). (S,R,S)-AHPC-C2-amide-benzofuranylmethyl-pyridine can also be applied to research related to various solid tumors and hematological malignancies, involving multiple cancer types such as colon cancer, breast cancer, ovarian cancer, non-small cell lung cancer, glioblastoma, and melanoma.
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Peptide CYP9
0 ImagesCat. No.: HY-P11914CAS No.: 3124554-07-7Peptide CYP9 is a head-to-tail cyclic peptide derived from Antimicrobial peptide YD (HY-P11913). Peptide CYP9 inhibits the activation of the TGF-β/Smad signaling pathway, including the phosphorylation of Smad2/3. Peptide CYP9 inhibits the activation of the MAPK signaling pathway, including the phosphorylation of ERK and p38. Peptide CYP9 inhibits epithelial-mesenchymal transition. Peptide CYP9 inhibits extracellular matrix synthesis. Peptide CYP9 can be used for the research of pulmonary fibrosis.
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CX-Se13
0 ImagesCat. No.: HY-187219CX-Se13 is an orally active pulmonary fibrosis inhibitor with anti-inflammatory and antioxidant activities. CX-Se13 regulates the Keap1/Nrf2/HO-1/NQO1, YAP/TAZ-TEAD, NF-κB p65 and TGF-β/Smads signaling pathways. CX-Se13 activates the cellular antioxidant defense system, restores redox balance, alleviates inflammatory responses, reduces collagen deposition, decreases pro-inflammatory cytokine levels and inhibits pathological progression. CX-Se13 can be used in studies related to pulmonary fibrosis.
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HIPK2-IN-2
0 ImagesCat. No.: HY-189141HIPK2-IN-2 is an orally active and selective HIPK2 inhibitor with an IC50 of 0.36 μM against HIPK2. HIPK2-IN-2 reduces HIPK2 protein expression levels. HIPK2-IN-2 inhibits the proliferation and migration of renal interstitial fibroblasts, alleviates renal tubular injury and collagen deposition, and suppresses TGF-β/Smad3-mediated profibrotic signaling pathways as well as TNF-α/NF-κB-mediated inflammatory signaling pathways in renal cells. HIPK2-IN-2 is used for the study of chronic kidney disease-associated renal fibrosis.
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HIPK2-IN-1
0 ImagesCat. No.: HY-189140HIPK2-IN-1 is an orally active and selective HIPK2 inhibitor with an IC50 of 0.56 μM. HIPK2-IN-1 exerts antifibrotic and anti-inflammatory activities. HIPK2-IN-1 binds to HIPK2, inhibits the downstream TGF‑β/Smad3, p53, and TNF‑α/NF‑κB signaling pathways, reduces the expression of fibrotic markers, suppresses cell proliferation and migration, and alleviates renal tubular injury and collagen deposition. HIPK2-IN-1 is used for the study of renal fibrosis associated with chronic kidney disease.
