Human Mothers Against Decapentaplegic Homolog 4 / MADH4 (SMAD4) CLIA Kit

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Description
Human Mothers Against Decapentaplegic Homolog 4 (Smad4/MADH4) Chemiluminescent Immunoassay (CLIA) Kit is a Chemiluminescent Immunoassay (CLIA) kit against Mothers Against Decapentaplegic Homolog 4 (Smad4/MADH4).
Documents del producto
Product specifications
Category | CLIA Kits |
Immunogen Target | Mothers Against Decapentaplegic Homolog 4 / MADH4 (SMAD4) |
Reactivity | Human |
Detection Method | Chemiluminescent |
Assay Data | Quantitative |
Assay Type | Sandwich |
Test Range | 62.5 pg/ml - 4000 pg/ml |
Sensitivity | 37.5 pg/ml |
Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
Size 1 | 96 tests |
Form | Lyophilized |
Tested Applications | CLIA |
Sample Type | Serum, plasma and other biological fluids. |
Availability | Shipped within 5-12 working days. |
Storage | Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual. |
Dry Ice | No |
Background | CLIA Kits SMAD4 |
Status | RUO |
Note | The validity for this kit is 6 months. This product is for research use only. The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments. Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein. |
Descripción
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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.
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anti- SMAD4 antibody
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anti- 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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