The SMAD3 (mothers against decapentaplegic homolog 3) gene is mapped to human chromosome 15q22.33. SMAD proteins contains three main domains : MH1 (MAD homology 1) - amino terminal domain (highly conserved), MH2 - carboxy terminal domain and a linker domain between the two domains. The MH1 domain of Smad3 serves as a DNA binding motif.(8)
Immunogen
The antiserum was produced against synthesized peptide derived from human Smad3 around the phosphorylation site of Ser204.
Immunogen Range: 170-219
Application
Anti-phospho-Smad3 (pSer204) antibody produced in rabbit has been used in western blot analysis.(7)
Biochem/physiol Actions
Smad3 (mothers against decapentaplegic homolog 3) protein identifies tandem repeats of the palindromic sequence GTCTAGAC, which is part of TGF-β (transforming growth factor β) signaling promoter region. Smad3 is associated with TGF-β (transforming growth factor beta) signaling pathway, a cellular process regulating the homeostasis, development, and repair of cartilage. It is known to induce extracellular matrix production. Smad proteins are responsible for the transduction of signals from cell surface to the nucleus. Phosphorylation of Smad3 controls tumor progression, inflammation, fibrosis, obesity and diabetes. Smad3 expression might be associated with the pathogenesis of osteoarthritis.
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Sodium tanshinone IIA sulfonate attenuates the transforming growth factor-beta1-induced differentiation of atrial fibroblasts into myofibroblasts in vitro
Yang L, et al.
International Journal of Molecular Medicine, 35(4), 1026-1032 (2015)
Signaling via Smad2 and Smad3 is dispensable for adult murine hematopoietic stem cell function in vivo
Billing M, et al.
Experimental Hematology, 55(6), 34-44 (2017)
Cardiovascular phenotype in Smad3 deficient mice with renovascular hypertension
Cardiac remodeling is one of the major risk factors for heart failure. In patients with type 2 diabetes, sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of the first hospitalization for heart failure, possibly through glucose-independent mechanisms in part, but
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