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48-602MAG
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Use Anti-Smad2/3 Antibody, clone C4T (Rabbit Monoclonal Antibody) validated in WB to detect Smad2/3 also known as Deletion target in pancreatic carcinoma 4, mothers against decapentaplegic homolog 4.
More>>Use Anti-Smad2/3 Antibody, clone C4T (Rabbit Monoclonal Antibody) validated in WB to detect Smad2/3 also known as Deletion target in pancreatic carcinoma 4, mothers against decapentaplegic homolog 4. Less<<
SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
MAD, mothers against decapentaplegic homolog 4 (Drosophila)
Mothers against DPP homolog 4
SMAD 4
SMAD family member 4
SMAD, mothers against DPP homolog 4
SMAD, mothers against DPP homolog 4 (Drosophila)
deleted in pancreatic carcinoma locus 4
mothers against decapentaplegic homolog 4
mothers against decapentaplegic, Drosophila, homolog of, 4
Background Information
Smad proteins are regulators of transcription which transduce signals from TGFβ Receptors. Smad proteins homotrimerize, and when activated, two distinct homotrimers assemble into a heterosextamer. Smad proteins fall into three classes. The receptor-regulated Smad proteins, Smad 1, 2, 3, 5, and 9 couple to specific receptors and are phosphorylated by those receptors. Phosphorylated receptor-regulated Smad proteins then bind to a co-Smad, such as Smad4/DPC4, and the complex moves to the nucleus where it associates with FAST-1 to stimulate target gene transcription. A third class of Smad proteins is the inhibitory group of Smad 6, 7, 8. Smad proteins have Mad-homology domains 1 and 2 (MH1 and MH2). MH1 domains are involved in DNA binding, while MH2 domains function in homotrimerization, receptor interaction and phosphorylation. Smad 4 mutations are frequently found in cancer, all of which cluster to the MH1 and MH2 domains of the protein. Those in the MH2 domain affect the ability of the protein to homotrimerize. The phosphorylation of Smad proteins is the regulatory signal in their activation, and can be monitored by the use of phosphorylation state-specific antibodies.
Use Anti-Smad2/3 Antibody, clone C4T (Rabbit Monoclonal Antibody) validated in WB to detect Smad2/3 also known as Deletion target in pancreatic carcinoma 4, mothers against decapentaplegic homolog 4.
Key Applications
Western Blotting
Biological Information
Immunogen
Fusion protein corresponding to amino acids 186-273 of human Smad2.
Epitope
a.a. 186-273
Clone
C4T
Concentration
Please refer to the Certificate of Analysis for the lot-specific concentration.
Host
Rabbit
Specificity
Recognizes Smad2, Mr 55-60 kDa and Smad3, Mr 50 kDa.
Species Reactivity
Human
Mouse
Rat
Species Reactivity Note
Human. Predicted to cross-react with mouse and rat based on conservation of immunogen sequence.
The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein mediates the signal of the transforming growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation. This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4.The association with SMAD4 is important for the translocation of this protein into the nucleus, where it binds to target promoters and forms a transcription repressor complex with other cofactors.This protein can also be phosphorylated by activin type 1 receptor kinase, and mediates the signal from the activin. Alternatively spliced transcript variants encoding the same protein have been observed.
FUNCTION:Common mediator of signal transduction by TGF-beta (transforming growth factor) superfamily; SMAD4 is the common SMAD (co-SMAD). Promotes binding of the SMAD2/SMAD4/FAST-1 complex to DNA and provides an activation function required for SMAD1 or SMAD2 to stimulate transcription. May act as a tumor suppressor. SUBUNIT STRUCTURE: May form trimers with receptor-regulated SMAD (R-SMAD). Found in a ternary complex composed of SMAD4, STK11 and STK11IP. Interacts with ATF2, COPS5, DACH1, MSG1, SKI, STK11, STK11IP and TRIM33. Associates with ZNF423 or ZNF521 in response to BMP2 leading to activate transcription of BMP target genes. Interacts with USP9X. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Note: Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with R-SMAD. PTM: Monoubiquitinated on Lys-519 by E3 ubiquitin-protein ligase TRIM33. Monoubiquitination hampers its ability to form a stable complex with activated SMAD2/3 resulting in inhibition of TGF-beta/BMP signaling cascade. INVOLVEMENT IN DISEASE: Defects in SMAD4 are a cause of pancreatic carcinoma [MIM:260350]. Defects in SMAD4 are a cause of juvenile polyposis syndrome (JPS) [MIM:174900]; also known as juvenile intestinal polyposis (JIP). JPS is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers. Defects in SMAD4 are a cause of juvenile polyposis/hereditary hemorrhagic telangiectasia syndrome (JP/HHT) [MIM:175050]. JP/HHT syndrome phenotype consists of the coexistence of juvenile polyposis (JIP) and hereditary hemorrhagic telangiectasia (HHT) [MIM:187300] in a single individual. JIP and HHT are autosomal dominant disorders with distinct and non-overlapping clinical features. The former, an inherited gastrointestinal malignancy predisposition, is caused by mutations in SMAD4 or BMPR1A, and the latter is a vascular malformation disorder caused by mutations in ENG or ACVRL1. All four genes encode proteins involved in the transforming-growth-factor-signaling pathway. Although there are reports of patients and families with phenotypes of both disorders combined, the genetic etiology of this association is unknown. Defects in SMAD4 may be a cause of colorectal cancer (CRC) [MIM:114500]. SEQUENCE SIMILARITIES:Belongs to the dwarfin/SMAD family. Contains 1 MH1 (MAD homology 1) domain. Contains 1 MH2 (MAD homology 2) domain.
Molecular Weight
~50-60 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blot on L6 lysates. Western Blotting Analysis: A 1:2,000 dilution of this antibody detected Smad2/3 in L6 cell lysate.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Storage and Shipping Information
Storage Conditions
Stable for 1 year at -20ºC from date of receipt. Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
