Product nameHuman Smad4 Matched Antibody Pair Kit
See all Smad4 kits
Assay typeELISA set
Range781.25 pg/ml - 50000 pg/ml
Species reactivityReacts with: Human
Matched Antibody Pair Kits include a capture and a biotinylated detector antibody pair, along with a calibrated protein standard, suitable for sandwich ELISA. The Matched Antibody Pair Kit can be used to quantify native and recombinant human Smad 4.
Matched antibody pair kits and reagents deliver consistent, specific, and sensitive results.
- Batch-to-batch consistency: only recombinant monoclonal antibodies are used in our matched antibody pairs.
- Specificity: antibody pairs are screened in plasma and serum to ensure specificity in complex samples.
- Sensitivity: benchmarked against commercially available antibody pairs to ensure equivalent or superior performance compared with the competition.
Additional buffers and plates are required for the assay. An accessory pack can be purchased which includes buffer reagents required to perform 10 x 96-well plate sandwich ELISAs (ab210905).
To receive an electronic copy of the Certificate of Analysis, please send an email with "CoA for matched antibody pair kit" in the subject line and the desired product number and lot number in the body of the email.
Tested applicationsSuitable for: ELISAmore details
Storage instructionsStore at -20°C. Please refer to protocols.
Components 10 x 96 tests 2 x 96 tests Human Smad4 Capture Antibody 1 x 100µg 1 x 20µg Human Smad4 Detector Antibody 1 x 25µg 1 x 5µg Human Smad4 Lyophilized Protein 1 vial 1 vial
FunctionCommon 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 syngernistic transcriptional activity in response to TGF-beta. May act as a tumor suppressor.
Involvement in diseaseDefects in SMAD4 are a cause of pancreatic cancer (PNCA) [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 similaritiesBelongs to the dwarfin/SMAD family.
Contains 1 MH1 (MAD homology 1) domain.
Contains 1 MH2 (MAD homology 2) domain.
DomainThe MH1 domain is required for DNA binding.
The MH2 domain is required for both homomeric and heteromeric interactions and for transcriptional regulation. Sufficient for nuclear import.
modificationsMonoubiquitinated 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. Deubiqitination by USP9X restores its competence to mediate TGF-beta signaling.
Cellular localizationCytoplasm. Nucleus. Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with R-SMAD.
- Information by UniProt
- (Small) Mothers Against Decapentaplegic
- Deleted in Pancreatic Carcinoma
- Deleted in Pancreatic Carcinoma 4
Our Abpromise guarantee covers the use of ab221430 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ELISA||Use at an assay dependent concentration.|
ab221430 has not yet been referenced specifically in any publications.