Anti-Smad3 (phospho S425) antibody (ab51177)
Key features and details
- Rabbit polyclonal to Smad3 (phospho S425)
- Suitable for: IHC-P
- Reacts with: Human
- Isotype: IgG
Overview
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Product name
Anti-Smad3 (phospho S425) antibody
See all Smad3 primary antibodies -
Description
Rabbit polyclonal to Smad3 (phospho S425) -
Host species
Rabbit -
Tested applications
Suitable for: IHC-Pmore details -
Species reactivity
Reacts with: Human -
Immunogen
Synthetic peptide corresponding to Human Smad3 aa 350-450 (phospho S425).
Database link: P84022 -
General notes
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Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at -20°C. Stable for 12 months at -20°C. -
Storage buffer
pH: 7.40
Preservative: 0.02% Sodium azide
Constituents: 50% Glycerol (glycerin, glycerine), 0.87% Sodium chloride, PBS
Without Mg+2 and Ca+2 -
Concentration information loading...
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Purity
Immunogen affinity purified -
Purification notes
The antibody was affinity purified from rabbit antiserum by affinity chromatography using epitope specific phosphopeptide. The antibody against non phosphopeptide was removed by chromatography using non phosphopeptide corresponding to the phosphorylation site. -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
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Recombinant Protein
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab51177 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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IHC-P | (1) |
Use at an assay dependent concentration.
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Notes |
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IHC-P
Use at an assay dependent concentration. |
Target
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Function
Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator. -
Involvement in disease
Colorectal cancer
Loeys-Dietz syndrome 3 -
Sequence similarities
Belongs to the dwarfin/SMAD family.
Contains 1 MH1 (MAD homology 1) domain.
Contains 1 MH2 (MAD homology 2) domain. -
Domain
The MH1 domain is required for DNA binding. Also binds zinc ions which are necessary for the DNA binding.
The MH2 domain is required for both homomeric and heteromeric interactions and for transcriptional regulation. Sufficient for nuclear import.
The linker region is required for the TGFbeta-mediated transcriptional activity and acts synergistically with the MH2 domain. -
Post-translational
modificationsPhosphorylated 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.
Ubiquitinated. Monoubiquitinated, leading to prevent DNA-binding. Deubiquitination by USP15 alleviates inhibition and promotes activation of TGF-beta target genes.
Poly-ADP-ribosylated by PARP1 and PARP2. ADP-ribosylation negatively regulates SMAD3 transcriptional responses during the course of TGF-beta signaling. -
Cellular localization
Cytoplasm. Nucleus. Cytoplasmic and nuclear in the absence of TGF-beta. On TGF-beta stimulation, migrates to the nucleus when complexed with SMAD4 (PubMed:15799969). Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1 (PubMed:16751101, PubMed:19289081). Co-localizes with LEMD3 at the nucleus inner membrane (PubMed:15601644). MAPK-mediated phosphorylation appears to have no effect on nuclear import (PubMed:19218245). PDPK1 prevents its nuclear translocation in response to TGF-beta (PubMed:17327236). - Information by UniProt
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Database links
- Entrez Gene: 4088 Human
- Omim: 603109 Human
- SwissProt: P84022 Human
- Unigene: 727986 Human
- Unigene: 742270 Human
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Alternative names
- DKFZP586N0721 antibody
- DKFZp686J10186 antibody
- hMAD 3 antibody
see all
Images
Datasheets and documents
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SDS download
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Datasheet download
References (16)
ab51177 has been referenced in 16 publications.
- Xu J et al. High-Dose TGF-ß1 Impairs Mesenchymal Stem Cell-Mediated Bone Regeneration via Bmp2 Inhibition. J Bone Miner Res 35:167-180 (2020). PubMed: 31487395
- Zhao H et al. PDCD5 inhibits osteosarcoma cell metastasis via targeting TGF-ß1/Smad signaling pathway and is associated with good prognosis. Am J Transl Res 11:1116-1128 (2019). PubMed: 30899411
- Feng J et al. RACK1 silencing attenuates renal fibrosis by inhibiting TGF-ß signaling. Int J Mol Med 40:1965-1970 (2017). PubMed: 29039466
- Seth B et al. Inhibition of the transforming growth factor-ß/SMAD cascade mitigates the anti-neurogenic effects of the carbamate pesticide carbofuran. J Biol Chem 292:19423-19440 (2017). PubMed: 28982980
- Zhu C et al. Plasminogen Activator Inhibitor 1 Promotes Immunosuppression in Human Non-Small Cell Lung Cancers by Enhancing TGF-?1 Expression in Macrophage. Cell Physiol Biochem 44:2201-2211 (2017). PubMed: 29253845