• Product name

  • Description

    Rabbit polyclonal to Smad4
  • Host species

  • Tested applications

    Suitable for: IP, IHC-P, WBmore details
  • Species reactivity

    Reacts with: Mouse, Human
    Predicted to work with: Rat, Cow, Pig
  • Immunogen

    Recombinant fragment corresponding to Human Smad4 aa 27-195.


    Database link: Q13485

  • Positive control

    • WB: SH-SY5Y, 3T3 and HepG2 whole cell lysate. IHC-P: Human colon cancer and kidney tissue. IP: Jurkat cells.



Our Abpromise guarantee covers the use of ab236321 in the following tested applications.

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

Application Abreviews Notes
IP 1/200 - 1/2000.
IHC-P 1/20 - 1/200.
WB 1/500 - 1/2000. Predicted molecular weight: 60 kDa.


  • 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

    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 localization

    Cytoplasm. Nucleus. Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with R-SMAD.
  • Information by UniProt
  • Database links

  • Alternative names

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


  • All lanes : Anti-Smad4 antibody (ab236321) at 1/500 dilution

    Lane 1 : SH-SY5Y (human neuroblastoma cell line from bone marrow) whole cell lysate
    Lane 2 : NIH/3T3 (mouse embryo fibroblast cell line) whole cell lysate

    All lanes : Goat polyclonal to rabbit IgG at 1/10000 dilution

    Predicted band size: 60 kDa

  • Paraffin-embedded human kidney tissue stained for Smad4 using ab236321 at 1/100 dilution in immunohistochemical analysis.

  • Paraffin-embedded human colon cancer tissue stained for Smad4 using ab236321 at 1/100 dilution in immunohistochemical analysis.

  • Anti-Smad4 antibody (ab236321) at 1/500 dilution + HepG2 (human liver hepatocellular carcinoma cell line) whole cell lysate

    Goat polyclonal to rabbit IgG at 1/10000 dilution

    Predicted band size: 60 kDa

  • Smad4 was immunoprecipitated from 0.5 mg Jurkat (human T cell leukemia cell line from peripheral blood) whole cell lysate with ab236321. 

    Lane 1: Rabbit control IgG instead of ab236321 in Jurkat whole cell lysate.
    Lane 2: ab236321 IP in Jurkat whole cell lysate.
    Lane 3: Jurkat whole cell lysate 10 µg (Input). 

    For western blotting, a HRP-conjugated Protein G antibody was used as the secondary antibody at 1/2000 dilution.




This product has been referenced in:

  • Bonan NF  et al. Inhibition of HGF/MET signaling decreases overall tumor burden and blocks malignant conversion in Tpl2-related skin cancer. Oncogenesis 8:1 (2019). Read more (PubMed: 30631034) »
  • Stojnev S  et al. Prognostic Impact of Canonical TGF-ß Signaling in Urothelial Bladder Cancer. Medicina (Kaunas) 55:N/A (2019). Read more (PubMed: 31238579) »
See all 2 Publications for this product

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