|Ig Isotype||Mouse IgG1|
|Product Name||Anti-Smad4(DPC4) Antibody (Monoclonal, DCS-46)|
|Storage & Handling||At -20°C for one year. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for a longer time.Avoid repeated freezing and thawing.|
|Description||Mouse IgG monoclonal antibody for Smad4 (DPC4), SMAD family member 4 (SMAD4) detection. Tested with WB, ICC in Human. No cross reactivity with other proteins.|
|Cite This Product||Anti-Smad4(DPC4) Antibody (Monoclonal, DCS-46) (Boster Biological Technology, Pleasanton CA, USA, Catalog # MA1089)|
|Contents/Buffer||Mouse ascites fluid, 1.2% sodium acetate, 2mg BSA, with 0.01mg NaN3 as preservative.|
|Immunogen||Recombinant human Smad4(DPC4).|
Assay Dilutions Overview
Immunocytochemistry , 1μg/ml, Human, -
Western blot, 2-4μg/ml, Human
Boster's Secondary Antibodies And IHC, WB Kits
The following reagents are used to generate the images below.Boster recommends Enhanced Chemiluminescent Kit with anti-Mouse IgG (EK1001) for Western blot, and HRP Conjugated anti-Mouse IgG Super Vision Assay Kit (SV0001-1) for ICC.
Images And Assay Conditions
Anti-Smad4(DPC4) antibody (monoclonal), MA1089, Western blotting
Lane 1: Rat Brain Tissue Lysate
Lane 2: Rat Brain Tissue Lysate
Protein Target Info (Source: Uniprot.org)
|Protein Name||Mothers against decapentaplegic homolog 4|
|Alternative Names||Mothers against decapentaplegic homolog 4;MAD homolog 4;Mothers against DPP homolog 4;SMAD family member 4;SMAD 4;Smad4;Smad4;Madh4;|
|Subcellular Localization||Cytoplasm . Nucleus . In the cytoplasm in the absence of ligand. Migration to the nucleus when complexed with R-SMAD. PDPK1 prevents its nuclear translocation. .|
|Molecular Weight||60469 MW|
*if product is indicated to react with multiple species, protein info is based on the human gene.
|Protein Function||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. 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. 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. 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 (By similarity). .|
|Research Areas||Apoptosis, Cancer, Cancer Metabolism, Cardiogenesis, Cardiovascular, Cytoplasmic, Epigenetics And Nuclear Signaling, Hypertrophy, Metabolism, Metabolism Processes, Nuclear Signaling, Nuclear Signaling Pathways, Oncoproteins/Suppressors, Pathways And Processes, Response To Hypoxia, Signal Transduction, Signaling Pathway, Stem Cells, Tgf Beta, Transcription Factors, Transcription Factors/Regulators, Tumor Suppressors, Vasculature
*You can search these to find other products in these research areas.
|Background||SMAD4 plays a pivotal role in signal transduction of the transforming growth factor beta superfamily cytokines by mediating transcriptional activation of target genes. Smad4 signalling in T cells is required for suppression of gastrointestinal cancer. Mutational inactivation of SMAD4 causes TGF-beta unresponsiveness and gave a basis for understanding the physiologic role of this gene in tumorigenesis. Mutations in DPC4(SMAD4) cause juvenile polyposis syndrome, but only account for a minority of cases.|
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