Human Smad4 Antibody Pair - BSA and Azide free (ab241847)
Key features and details
- Unconjugated capture and detector antibodies
- Adaptable to any antibody pair-based assay format
- Antibody concentration ~ 1 mg/ml
- BSA and azide free buffer - ready for conjugation
- Reacts with: Human
Overview
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Product name
Human Smad4 Antibody Pair - BSA and Azide free
See all Smad4 kits -
Assay type
ELISA set -
Range
781.25 pg/ml - 50000 pg/ml -
Species reactivity
Reacts with: Human -
Product overview
The Antibody Pair can be used to quantify Human Smad4. BSA and Azide free antibody pairs include unconjugated capture and detector antibodies suitable for sandwich ELISAs. The antibodies are provided at an approximate concentration of 1 mg/ml as measured by the protein A280 method. The recommended antibody orientation is based on internal optimization for ELISA-based assays. Antibody orientation is assay dependent and needs to be optimized for each assay type. Both capture and detector antibodies are rabbit monoclonal antibodies delivering consistent, specific, and sensitive results.
For additional information on the performance of the antibody pair, see the equivalent SimpleStep ELISA® Kit (ab253211), which uses the same antibodies. However, due to differences in their formulation, this antibody pair cannot be used with the consumables provided with our SimpleStep ELISA Kits. Please note that the range provided for the pairs is only an estimation based on the performance of the related product using the same antibody pair. Performance of the antibody pair will depend on the specific characteristics of your assay. We guarantee the product works in sandwich ELISA, but we do not guarantee the sensitivity or dynamic range of the antibody pair in your assay.
Download SDS here.
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Tested applications
Suitable for: Sandwich ELISAmore details -
Platform
Reagents
Properties
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Storage instructions
Store at +4°C. Please refer to protocols. -
Carrier free
Yes -
Components 10 x 96 tests Human Smad4 Capture Antibody (unconjugated) 1 x 100µg Human Smad4 Detector Antibody (unconjugated) 1 x 100µg -
Research areas
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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 syngernistic transcriptional activity in response to TGF-beta. May act as a tumor suppressor. -
Involvement in disease
Defects 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 similarities
Belongs to the dwarfin/SMAD family.
Contains 1 MH1 (MAD homology 1) domain.
Contains 1 MH2 (MAD homology 2) domain. -
Domain
The 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. -
Post-translational
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 localization
Cytoplasm. Nucleus. Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with R-SMAD. - Information by UniProt
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Alternative names
- (Small) Mothers Against Decapentaplegic
- Deleted in Pancreatic Carcinoma
- Deleted in Pancreatic Carcinoma 4
see all -
Database links
- Entrez Gene: 4089 Human
- Omim: 600993 Human
- SwissProt: Q13485 Human
- Unigene: 75862 Human
Images
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Sandwich ELISA - Human Smad4 Antibody Pair - BSA and Azide free (ab241847)To learn more about the advantages of recombinant antibodies see here.
