|Application ||WB, IHC|
|Calculated MW||48081 Da|
|Other 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, SMAD3, MADH3|
|Target/Specificity||A synthetic peptide corresponding to the internal region of human Smad3 was used as immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Smad3 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|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.|
|Cellular Location||Cytoplasm. Nucleus. Note=Cytoplasmic and nuclear in the absence of TGF-beta. On TGF-beta stimulation, migrates to the nucleus when complexed with SMAD4. Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1. Co-localizes with LEMD3 at the nucleus inner membrane MAPK-mediated phosphorylation appears to have no effect on nuclear import. PDPK1 prevents its nuclear translocation in response to TGF-beta|
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Provided below are standard protocols that you may find useful for product applications.
Smad proteins belong to a group of intracellular signal transducers and downstream effectors of TGF-β/BMP Signaling. The family consists of nine members that are highly conserved in the N- and C-terminal regions (1). Smad3 is a key component in intracellular signaling of transforming growth factor beta (TGF-β), an inhibitor for tumor cell proliferation (2). Smad3 is activated by activin/TGF-β receptors, which form a heteromeric complex with Smad4, translocating to the nucleus and regulating the expression of TGF- β target genes. Interaction of Smad3 with Akt, can initiate TGF- β induced apoptosis and cell cycle arrest (3). Smad3 expression may be critical in tumor suppression in early stages of gastric carcinogenesis (4).
1. Yang X, et al. Devel Biol 95:3667-3672, 1998.
2. Preobrazhenska O, et al. Oncogene 21:5660-5664, 2002.
3. Qing C et al. J Biol Chem 275:38802-38812, 2000.
4. Han SU, et al. Oncogene 23:1333-1341, 2004.
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