|Application ||IHC-P, WB, E|
|Other Accession||P84025, P84024, Q8BUN5, P84023|
|Predicted||Chicken, Mouse, Pig, Rat|
|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||This SMAD3 Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S213 of human SMAD3.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Phospho-SMAD3(S213) 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.
SMAD3, a receptor regulated SMAD (R-SMAD) is a transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinase. SMAD3 is estimated to account for at least 80% of all TGF-beta-mediated response. Activated type I receptor phosphorylates receptor-activated SMADS (RSMADS) at their c-terminal two extreme serines in the SSXS motif. The phosphorylated R-SMAD translocate into nucleus, where they regulate transcription of target genes. SMAD3 signal transduction appears to be important in the rgulation of muscle-specific genes. Loss of SMAD3 is a feature of pediatric T-cell lymphoblastic leukemia, while upregulation of SMAD3 may be responsible for TGFB hyperresponsiveness observed in scleroderma.
Imoto, S., et al., FEBS Lett. 579(13):2853-2862 (2005).
Dubrovska, A., et al., Oncogene 24(14):2289-2297 (2005).
Furumatsu, T., et al., J. Biol. Chem. 280(9):8343-8350 (2005).
Kobayashi, T., et al., Biochem. Biophys. Res. Commun. 327(2):393-398 (2005).
Kamaraju, A.K., et al., J. Biol. Chem. 280(2):1024-1036 (2005).
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