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Rabbit Polyclonal Phospho-Smad3 (T179) antibody (STJ90905)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IHC, ELISA
Recommended dilution: WB 1:500-1:2000; IHC 1:100-1:300; ELISA 1:10000;
Recommended protocols: check protocols
Click or hover above images to see image description for Smad3 (phospho Thr179) Polyclonal Antibody.
Check alternative names for the antibodyExpand
SMAD3 antibody, MADH3 antibody,|DKFZP586N0721 antibody|SMAD 3 antibody|SMAD antibody|SMAD family member 3 antibody|SMAD, mothers against DPP homolog 3 antibody|Smad3 antibody|SMAD3_HUMAN antibody|Anti-Smad3 antibody [EP568Y] (ab40854)
SCBT cat No: sc-11769|sc-130218|sc-514317|sc-165305|sc-515132|sc-74864|sc-390878|sc-100454|sc-100455|sc-71790|sc-56746|
Smad3 (phospho Thr179) Polyclonal Antibody
|Catalogue No.|| |
Human, Mouse, Rat
Phospho-Smad3 (T179) Polyclonal Antibody detects endogenous levels of Smad3 protein only when phosphorylated at T179.
Synthesized phospho-peptide derived from Smad3 (phospho Thr179) at AA range 120-200
WB, IHC, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IHC 1:100-1:300; ELISA 1:10000;
|Molecular weight|| |
Smad3 (phospho Thr179) Antibody was tube-contained. Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Smad3 (phospho Thr179) Antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Mothers against decapentaplegic homolog 3 antibody, MAD homolog 3 antibody, Mad3 antibody, Mothers against DPP homolog 3 antibody, hMAD-3 antibody, JV15-2 antibody, SMAD family member 3 antibody, SMAD 3 antibody, Smad3 antibody, hSMAD3 antibody
|Protein names|| |
Mothers against decapentaplegic homolog 3 , MAD homolog 3 , Mad3 , Mothers against DPP homolog 3 , hMAD-3 , JV15-2 , SMAD family member 3 , SMAD 3 , Smad3 , hSMAD3
|Protein 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 (CRC) [MIM:114500]: A complex disease characterized by malignant lesions arising from the inner wall of the large intestine (the colon) and the rectum. Genetic alterations are often associated with progression from premalignant lesion (adenoma) to invasive adenocarcinoma. Risk factors for cancer of the colon and rectum include colon polyps, long-standing ulcerative colitis, and genetic family history. . Note: The disease may be caused by mutations affecting the gene represented in this entry.; Loeys-Dietz syndrome 3 (LDS3) [MIM:613795]: An aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation. . Note: The disease is caused by mutations affecting the gene represented in this entry. SMAD3 mutations have been reported to be also associated with thoracic aortic aneurysms and dissection (TAAD) (PubMed:21778426). This phenotype is distinguised from LDS3 by having aneurysms restricted to thoracic aorta. As individuals carrying these mutations also exhibit aneurysms of other arteries, including abdominal aorta, iliac, and/or intracranial arteries (PubMed:21778426), they have been classified as LDS3 by the OMIM resource. .
|Protein sequence and 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. / Belongs to the dwarfin/SMAD family. / Contains 1 MH1 (MAD homology 1) domain. / Contains 1 MH2 (MAD homology 2) domain.
|Protein post-translational modifications|| |
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 G1/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.
|Protein cellular localization|| |
Cytoplasm / Nucleus
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St John’s Laboratory Ltd.
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