Smad3 Antibody (YA5458)
(Synonyms: SMAD3)Smad3 Antibody (YA5458) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to Smad3.
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Host:
Mouse
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Application:
WB, ICC/IF, ELISA
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Reactivity :
Human, Rat, Mouse
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Formulation:
Supplied in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
|---|---|---|
| Dilution Ratio | 1:1000-2000 | 1:50-200 |
Product Details
Smad3 Antibody (YA5458) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to Smad3.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Rat, Mouse
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Observed Molecular WeightObserved band size: 52 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
Synthetic Peptide of Smad3 at AA range of 350-430
affinity chromatography.
Non-conjugated
Unmodified
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
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].
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Subcellular Localization
Cytoplasm; Nucleus
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Isoforms & Post-Translational Modification
P84022 has 4 isomers: P84022-1: 48081 Da (predicted); P84022-2: 43237 Da (predicted); P84022-3: 35895 Da (predicted); P84022-4: 25722 Da (predicted).
Phosphorylated on serine and threonine residues. Enhanced phosphorylation in the linker region on Thr-179, Ser-204 and Ser-208 on EGF and TGF-beta treatment. Ser-208 is the main site of MAPK-mediated phosphorylation. CDK-mediated phosphorylation occurs in a cell-cycle dependent manner and inhibits both the transcriptional activity and antiproliferative functions of SMAD3. This phosphorylation is inhibited by flavopiridol. Maximum phosphorylation at the G(1)/S junction. Also phosphorylated on serine residues in the C-terminal SXS motif by TGFBR1 and ACVR1. TGFBR1-mediated phosphorylation at these C-terminal sites is required for interaction with SMAD4, nuclear location and transactivational activity, and appears to be a prerequisite for the TGF-beta mediated phosphorylation in the linker region. Dephosphorylated in the C-terminal SXS motif by PPM1A. This dephosphorylation disrupts the interaction with SMAD4, promotes nuclear export and terminates TGF-beta-mediated signaling. Phosphorylation at Ser-418 by CSNK1G2/CK1 promotes ligand-dependent ubiquitination and subsequent proteasome degradation, thus inhibiting SMAD3-mediated TGF-beta responses. Phosphorylated by PDPK1;Acetylation in the nucleus by EP300 in the MH2 domain regulates positively its transcriptional activity and is enhanced by TGF-beta;Poly-ADP-ribosylated by PARP1 and PARP2. ADP-ribosylation negatively regulates SMAD3 transcriptional responses during the course of TGF-beta signaling;Ubiquitinated. Monoubiquitinated, leading to prevent DNA-binding (PubMed:21947082). Deubiquitination by USP15 alleviates inhibition and promotes activation of TGF-beta target genes (PubMed:21947082). Ubiquitinated by RNF111, leading to its degradation: only SMAD3 proteins that are 'in use' are targeted by RNF111, RNF111 playing a key role in activating SMAD3 and regulating its turnover (By similarity). Undergoes STUB1-mediated ubiquitination and degradation (PubMed:24613385) -
Subunit
Monomer; in the absence of TGF-beta (PubMed:9670020). Homooligomer; in the presence of TGF-beta (PubMed:9670020).
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SwissProt ID
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Synonyms
SMAD3
Documentation
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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