Overview

Description

  • NatureRecombinant
  • SourceEscherichia coli
  • Amino Acid Sequence
    • SpeciesHuman
    • SequenceMGSSHHHHHH SSGLVPRGSH MDNMSITNTP TSNDACLSIV HSLMCHRQGG ESETFAKRAI ESLVKKLKEK KDELDSLITA ITTNGAHPSK CVTIQRTLDG RLQVAGRKGF PHVIYARLWR WPDLHKNELK HVKYCQYAFD LKCDSVCVNP YHYERVVSPG IDLSGLTLQS NAPSSMMVKD EYVHDFEGQP SLSTEGHSIQ TIQHPPSNRA STETYSTPAL LAPSESNATS TANFPNIPVA STSQPASILG GSHSEGLLQI ASGPQPGQQQ NGFTGQPATY HHNSTTTWTG SRTAPYTPNL PHHQNGHLQH HPPMPPHPGH YWPVHNELAF QPPISNHPAP EYWCSIAYFE MDVQVGETFK VPSSCPIVTV DGYVDPSGGD RFCLGQLSNV HRTEAIERAR LHIGKGVQLE CKGEGDVWVR CLSDHAVFVQ SYYLDREAGR APGDAVHKIY PSAYIKVFDL RQCHRQMQQQ AATAQAAAAA QAAAVAGNIP GPGSVGGIAP AISLSAAAGI GVDDLRRLCI LRMSFVKGWG PDYPRQSIKE TPCWIEIHLH RALQLLDEVL HTMPIADPQP LD

Specifications

Our Abpromise guarantee covers the use of ab81764 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

  • Applications

    SDS-PAGE

    Western blot

    Electrophoretic Mobility Shift Assay

  • Purity> 90 % SDS-PAGE.

  • FormLiquid
  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.

    Preservative: None
    Constituents: 20% Glycerol, 20mM Tris HCl, pH 8.0

General Info

  • Alternative names
    • (Small) Mothers Against Decapentaplegic
    • Deleted in Pancreatic Carcinoma
    • Deleted in Pancreatic Carcinoma 4
    • Deleted in pancreatic carcinoma locus 4
    • Deletion target in pancreatic carcinoma 4
    • DPC 4
    • DPC4
    • hSMAD4
    • JIP
    • MAD homolog 4
    • MAD mothers against decapentaplegic Drosophila homolog 4
    • MAD mothers against decapentaplegic homolog 4
    • MADH 4
    • MADH4
    • Med
    • Medea
    • Mothers against decapentaplegic homolog 4
    • Mothers against decapentaplegic, Drosophila, homolog of, 4
    • Mothers against DPP homolog 4
    • MYHRS
    • OTTHUMP00000163548
    • SMA- and MAD-related protein 4
    • SMAD 4
    • SMAD family member 4
    • SMAD mothers against DPP homolog 4
    • SMAD4
    • SMAD4_HUMAN
    see all
  • 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.
  • Post-translational
    modifications
    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. 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

Recombinant Human Smad4 protein images

  • ab81764 on 15% SDS-PAGE (3µg)
  • Anti-Smad4 antibody (ab65217) at 1/500 dilution + Recombinant Human Smad4 protein (ab81764) at 0.1 µg

    Secondary
    Goat polyclonal to Rabbit IgG - H&L - Pre-Adsorbed (HRP) (ab65484) at 1/5000 dilution
    Developed using the ECL technique

    Performed under reducing conditions.

    Exposure time : 8 minutes

References for Recombinant Human Smad4 protein (ab81764)

This product has been referenced in:
  • Jiang Y  et al. Phosphatase PRL-3 is a direct regulatory target of TGFbeta in colon cancer metastasis. Cancer Res 71:234-44 (2011). EMSA . Read more (PubMed: 21084277) »

See 1 Publication for this product

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Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"