Recombinant Human SMAD4
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Product specifications
| Category | Proteins and Peptides |
| Host | E.Coli |
| Reactivity | Human |
| Assay Data | Centrifuge the vial before opening, reconstitute in sterile distilled water to a concentration of 0.1-1 mg/ml by gently pipetting 2-3 times, don't vortex. |
| Recommended Dilution | ¥ |
| Isotype | ¥ |
| Clone ID | ¥ |
| Observed MW | 25.6 kDa |
| Expression | 13-227 |
| Purity | Greater than 90% as determined by SDS-PAGE. |
| Size 1 | 50μg |
| Size 2 | 200μg |
| Size 3 | 1mg |
| Form | Lyophilized powder |
| Tested Applications | Western Blot, ELISA |
| Buffer | Lyophilized from a 0.2 μm filtered solution in 10 mM Hepes, 500 mM NaCl with 5% trehalose, pH 7.4. |
| Availability | 7 days |
| Storage | The lyophilized protein is stable at -20 °C for up to 1 year. After reconstitution, the protein solution is stable at -20 to -80 °C for 3 months or 1 week at 2 to 8 °C under sterile conditions. For extended storage, it is recommended to further dilute in working aliquots, avoid repeated freeze/thaw cycle. |
| UniProt ID | Q13485 |
| Alias | DPC4, hSMAD4, JIP, MAD homolog 4, MADH4, Mothers against DPP homolog 4, SMAD 4, SMAD family member 4, SMAD4 |
| Background | Protein SMAD4 |
| Status | RUO |
| Note | Tag : N-terminal His Tag |
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SMAD4 antibody
In muscle physiology, plays a central role in the balance between atrophy and hypertrophy. When recruited by MSTN, promotes atrophy response via phosphorylated SMAD2/4. MSTN decrease causes SMAD4 release and subsequent recruitment by the BMP pathway to promote hypertrophy via phosphorylated SMAD1/5/8. Acts synergistically with SMAD1 and YY1 in bone morphogenetic protein(BMP)-mediated cardiac-specific gene expression. Binds to SMAD binding elements(SBEs)(5'-GTCT/AGAC-3') within BMP response element(BMPRE) of cardiac activating regions(By similarity). Common SMAD(co-SMAD) is the coactivator and mediator of signal transduction by TGF-beta(transforming growth factor). Component of the heterotrimeric SMAD2/SMAD3-SMAD4 complex that forms in the nucleus and is required for the TGF-mediated signaling. Promotes binding of the SMAD2/SMAD4/FAST-1 complex to DNA and provides an activation function required for SMAD1 or SMAD2 to stimulate transcription. Component of the multimeric SMAD3/SMAD4/JUN/FOS complex which forms at the AP1 promoter site; required for synergistic transcriptional activity in response to TGF-beta. May act as a tumor suppressor. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.
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In muscle physiology, plays a central role in the balance between atrophy and hypertrophy. When recruited by MSTN, promotes atrophy response via phosphorylated SMAD2/4. MSTN decrease causes SMAD4 release and subsequent recruitment by the BMP pathway to promote hypertrophy via phosphorylated SMAD1/5/8. Acts synergistically with SMAD1 and YY1 in bone morphogenetic protein(BMP)-mediated cardiac-specific gene expression. Binds to SMAD binding elements(SBEs)(5'-GTCT/AGAC-3') within BMP response element(BMPRE) of cardiac activating regions(By similarity). Common SMAD(co-SMAD) is the coactivator and mediator of signal transduction by TGF-beta(transforming growth factor). Component of the heterotrimeric SMAD2/SMAD3-SMAD4 complex that forms in the nucleus and is required for the TGF-mediated signaling. Promotes binding of the SMAD2/SMAD4/FAST-1 complex to DNA and provides an activation function required for SMAD1 or SMAD2 to stimulate transcription. Component of the multimeric SMAD3/SMAD4/JUN/FOS complex which forms at the AP1 promoter site; required for synergistic transcriptional activity in response to TGF-beta. May act as a tumor suppressor. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.
Ver ProductoSMAD4 antibody
In muscle physiology, plays a central role in the balance between atrophy and hypertrophy. When recruited by MSTN, promotes atrophy response via phosphorylated SMAD2/4. MSTN decrease causes SMAD4 release and subsequent recruitment by the BMP pathway to promote hypertrophy via phosphorylated SMAD1/5/8. Acts synergistically with SMAD1 and YY1 in bone morphogenetic protein(BMP)-mediated cardiac-specific gene expression. Binds to SMAD binding elements(SBEs)(5'-GTCT/AGAC-3') within BMP response element(BMPRE) of cardiac activating regions(By similarity). Common SMAD(co-SMAD) is the coactivator and mediator of signal transduction by TGF-beta(transforming growth factor). Component of the heterotrimeric SMAD2/SMAD3-SMAD4 complex that forms in the nucleus and is required for the TGF-mediated signaling. Promotes binding of the SMAD2/SMAD4/FAST-1 complex to DNA and provides an activation function required for SMAD1 or SMAD2 to stimulate transcription. Component of the multimeric SMAD3/SMAD4/JUN/FOS complex which forms at the AP1 promoter site; required for synergistic transcriptional activity in response to TGF-beta. May act as a tumor suppressor. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.
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