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SMAD1 Protein, Human, Recombinant (GST)

Catalog No. TMPJ-01129

SMAD Family Member 1 (SMAD1) is a member of the dwarfin/SMAD family. SMAD1 has the highest expression in the heart and skeletal muscle, containing one MAD homology 1 domain and one MAD homology 2 domain, As a transcriptional modulator SMAD 1 is activated by bone morphogenetic proteins type 1 receptor kinase. Defects in SMAD1 may cause primary pulmonary hypertension (PPH1), characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure and death.

SMAD1 Protein, Human, Recombinant (GST)

SMAD1 Protein, Human, Recombinant (GST)

Catalog No. TMPJ-01129
SMAD Family Member 1 (SMAD1) is a member of the dwarfin/SMAD family. SMAD1 has the highest expression in the heart and skeletal muscle, containing one MAD homology 1 domain and one MAD homology 2 domain, As a transcriptional modulator SMAD 1 is activated by bone morphogenetic proteins type 1 receptor kinase. Defects in SMAD1 may cause primary pulmonary hypertension (PPH1), characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure and death.
Pack SizePriceAvailabilityQuantity
10 μg$1847-10 days
50 μg$5457-10 days
500 μg$1,9007-10 days
1 mg$2,7307-10 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
SMAD Family Member 1 (SMAD1) is a member of the dwarfin/SMAD family. SMAD1 has the highest expression in the heart and skeletal muscle, containing one MAD homology 1 domain and one MAD homology 2 domain, As a transcriptional modulator SMAD 1 is activated by bone morphogenetic proteins type 1 receptor kinase. Defects in SMAD1 may cause primary pulmonary hypertension (PPH1), characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure and death.
Species
Human
Expression System
E. coli
TagN-GST
Accession NumberQ15797
Synonyms
Transforming Growth Factor-β-Signaling Protein 1,Transforming Growth Factor-Beta-Signaling Protein 1,SMAD1,SMAD Family Member 1,SMAD 1,Mothers Against DPP Homolog 1,Mothers Against Decapentaplegic Homolog 1,Mad-Related Protein 1,MADR1,MADH1,MAD Homolog 1,JV4-1,hSMAD1,BSP-1,BSP1
Amino Acid
Met1-Ser465
Construction
Met1-Ser465
Protein Purity
Greater than 95% as determined by reducing SDS-PAGE. (QC verified)
Molecular Weight58-80 KDa (reducing condition)
Endotoxin< 0.1 ng/µg (1 EU/µg) as determined by LAL test.
FormulationLyophilized from a solution filtered through a 0.22 μm filter, containing 20 mM Tris-HCl, 150 mM NaCl, pH 8.0.
Reconstitution
Reconstitute the lyophilized protein in distilled water. The product concentration should not be less than 100 μg/ml. Before opening, centrifuge the tube to collect powder at the bottom. After adding the reconstitution buffer, avoid vortexing or pipetting for mixing.
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.
ShippingIn general, Lyophilized powders are shipping with blue ice. Solutions are shipping with dry ice.
Research Background
SMAD Family Member 1 (SMAD1) is a member of the dwarfin/SMAD family. SMAD1 has the highest expression in the heart and skeletal muscle, containing one MAD homology 1 domain and one MAD homology 2 domain, As a transcriptional modulator SMAD 1 is activated by bone morphogenetic proteins type 1 receptor kinase. Defects in SMAD1 may cause primary pulmonary hypertension (PPH1), characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure and death.

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Keywords