Anti-Smad4(DPC4) Antibody (Monoclonal, DCS-46)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, ICC |
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Primary Accession | O70437 |
Host | Mouse |
Isotype | Mouse IgG1 |
Reactivity | Human |
Clonality | Monoclonal |
Format | Lyophilized |
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. |
Reconstitution | Add 1ml of PBS buffer will yield a concentration of 100ug/ml. |
Gene ID | 50554 |
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Other Names | Mothers against decapentaplegic homolog 4, MAD homolog 4, Mothers against DPP homolog 4, SMAD family member 4, SMAD 4, Smad4, Smad4, Madh4 |
Calculated MW | 60469 MW KDa |
Application Details | Immunocytochemistry , 1 µg/ml, Human, - Western blot, 2-4 µg/ml, Human |
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. . |
Protein Name | Mothers against decapentaplegic homolog 4 |
Contents | Mouse ascites fluid, 1.2% sodium acetate, 2mg BSA, with 0.01mg NaN3 as preservative. |
Clone Names | DCS-46 |
Immunogen | Recombinant human Smad4(DPC4). |
Purification | Ascites |
Cross Reactivity | No cross reactivity with other proteins |
Storage | At -20˚C for one year. After r˚Constitution, 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. |
Sequence Similarities | Belongs to the dwarfin/SMAD family. |
Name | Smad4 |
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Synonyms | Madh4 |
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). |
Cellular Location | Cytoplasm {ECO:0000250|UniProtKB:Q13485}. Nucleus {ECO:0000250|UniProtKB:Q13485}. Note=In the cytoplasm in the absence of ligand. Migration to the nucleus when complexed with R-SMAD. PDPK1 prevents its nuclear translocation. {ECO:0000250|UniProtKB:Q13485} |
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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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