This webpage contains legacy information. The product is either no longer available from the supplier or has been delisted at Labome.
product summary
company name :
Boster
product type :
antibody
product name :
Anti-Smad4(DPC4) Antibody (Monoclonal, DCS-46)
catalog :
MA1089
quantity :
100μg/vial
clonality :
monoclonal
host :
mouse
conjugate :
nonconjugated
clone name :
DCS-46

The same clone is also sold as:
reactivity :
human, rat
application :
western blot, immunocytochemistry
product information
SKU :
MA1089
Product Name :
Anti-Smad4(DPC4) Antibody (Monoclonal, DCS-46)
Size :
100μg/vial
Clonality :
Monoclonal
Clone Number :
DCS-46
Host :
Mouse
Reactivity :
Human
Predicted Reactivity :
Bovine, Monkey
Application(s) :
ICC, WB
Application Details :
Immunocytochemistry , 1µg/ml, Human Western blot, 2-4µg/ml, Human.
Application Notes :
Other applications have not been tested. Optimal dilutions should be determined by end users.
Description :
Boster Bio Anti-Smad4 (DPC4) Antibody (Monoclonal, DCS-46) catalog # MA1089. Tested in ICC, WB applications. This antibody reacts with Human.
Concentration :
Adding 1 ml of PBS buffer will yield a concentration of 100 μg/ml.
Gene Name :
SMAD4
Uniprot ID :
O70437
Immunogen :
Recombinant human Smad4 (DPC4).
Form :
Lyophilized
Contents :
Mouse ascites fluid, 1.2% sodium acetate, 2mg BSA, with 0.01mg NaN3 as preservative.
Purification :
Ascites
Cross-reactivity :
No cross reactivity with other proteins
Isotype :
Mouse IgG1
Storage :
Store at -20˚C for one year from date of receipt. After reconstitution, at 4˚C for one month. It can also be aliquotted and stored frozen at -20˚C for six months. Avoid repeated freeze-thaw cycles.
Reconstitution :
Add 1ml of PBS buffer will yield a concentration of 100ug/ml.
Gene Full Name :
Mothers against decapentaplegic homolog 4
Synonyms :
Mothers against decapentaplegic homolog 4; MAD homolog 4; Mothers against DPP homolog 4; SMAD family member 4; SMAD 4; Smad4; Smad4; Madh4;
Protein Name :
Mothers against decapentaplegic homolog 4
Molecular Weight :
60469 MW
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).
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.
Recommended Detection Systems :
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.
Sequence Similarities :
Belongs to the dwarfin/SMAD family.
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.
Research Category :
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
company information
Boster
3942 B Valley Ave
Pleasanton, CA 94566
boster@bosterbio.com
https://www.bosterbio.com
925.485.4527
headquarters: USA
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