SMAD3 Protein, Human, Recombinant (His & Flag)

Catalog No. TMPJ-00271

Mothers against decapentaplegic homolog 3(SMAD3) is a cytoplasm protein which belongs to the dwarfin/SMAD family. Smad proteins undergo rapid nuclear translocation upon stimulation by transforming growth factor and in so doing transduce the signal into the nucleus. Receptor-regulated SMAD is an intracellular signal transducer and transcriptional modulator activated by TGF-beta and activin type 1 receptor kinases. SMAD3 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. It also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. SMAD3 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.

SMAD3 Protein, Human, Recombinant (His & Flag)

Catalog No. TMPJ-00271

Pack Size	Price	Availability
10 μg	$110	7-10 days
50 μg	$310	7-10 days
500 μg	$1,390	7-10 days
1 mg	$1,980	7-10 days

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Product Information

Biological Activity	Activity has not been tested. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first.
Description	Mothers against decapentaplegic homolog 3(SMAD3) is a cytoplasm protein which belongs to the dwarfin/SMAD family. Smad proteins undergo rapid nuclear translocation upon stimulation by transforming growth factor and in so doing transduce the signal into the nucleus. Receptor-regulated SMAD is an intracellular signal transducer and transcriptional modulator activated by TGF-beta and activin type 1 receptor kinases. SMAD3 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. It also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. SMAD3 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.
Species	Human
Expression System	E. coli
Tag	N-6xHis-Flag
Accession Number	P84022
Synonyms	SMAD3,SMAD family member 3,SMAD 3,Mothers against DPP homolog 3,Mothers against decapentaplegic homolog 3,MADH3,Mad3,MAD homolog 3,JV15-2,hSMAD3,hMAD-3
Amino Acid	Ser2-Ser425
Construction	Ser2-Ser425
Protein Purity	Greater than 85% as determined by reducing SDS-PAGE. (QC verified)
Molecular Weight	50-60 KDa (reducing condition)
Endotoxin	< 1 EU/μg by the LAL method.
Formulation	Supplied as a 0.2 μm filtered solution of 20 mM Tris-HCl, 500 mM NaCl, 10% Glycerol, 2 mM EDTA, pH 8.0.
Stability & Storage	Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
Shipping	Shipping with blue ice.
Research Background	Mothers against decapentaplegic homolog 3(SMAD3) is a cytoplasm protein which belongs to the dwarfin/SMAD family. Smad proteins undergo rapid nuclear translocation upon stimulation by transforming growth factor and in so doing transduce the signal into the nucleus. Receptor-regulated SMAD is an intracellular signal transducer and transcriptional modulator activated by TGF-beta and activin type 1 receptor kinases. SMAD3 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. It also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. SMAD3 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.