Smad3 Antibody (YA4140)
(Synonyms: MADH3; JV15-2; HSPC193; HsT17436; MGC60396; DKFZp586N0721; DKFZp686J10186; SMAD3)Smad3 Antibody (YA4140) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to Smad3.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, ICC/IF, ELISA
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Reactivity :
Human, Mouse
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Formulation:
Supplied in PBS with 0.05% 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 |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:1000 | 1:10000 |
Product Details
Smad3 Antibody (YA4140) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to Smad3.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse
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Observed Molecular WeightObserved band size: 55 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.
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Calculated Molecular Weight Predicted band size: 48 kDa
Purified recombinant fragment of human SMAD3 aa 1-230.
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS with 0.05% 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
MADH3; JV15-2; HSPC193; HsT17436; MGC60396; DKFZp586N0721; DKFZp686J10186; 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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