• Product name

    Anti-Smad4 antibody - N-terminal
    See all Smad4 primary antibodies
  • Description

    Rabbit polyclonal to Smad4 - N-terminal
  • Host species

  • Tested applications

    Suitable for: WB, IHC-Pmore details
  • Species reactivity

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

    Synthetic peptide corresponding to Human Smad4 aa 97-113 (N terminal).


    Database link: Q13485

  • Positive control

    • Rat Skeletal Muscle Tissue Lysate, A549 and U87 Cell Lysates; Human Lung Cancer Tissue; Rat Intestine and Brain Tissues.



Our Abpromise guarantee covers the use of ab191026 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
WB Use a concentration of 0.1 - 0.5 µg/ml. Predicted molecular weight: 60 kDa.

The detection limit for Smad4.is approximately 2.5ng/lane under reducing conditions

IHC-P Use a concentration of 0.5 - 1 µg/ml. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.


  • 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 - N-terminal (ab191026) at 0.5 µg/ml

    Lane 1 : Rat Skeletal Muscle Tissue Lysate
    Lane 2 : A549 Cell Lysate
    Lane 3 : U87 Cell Lysate

    Predicted band size: 60 kDa

  • Immunohistochemical analysis of paraffin-embedded Rat Brain Tissue labeling Smad4 with ab191026 at 1 µg/ml.

  • Immunohistochemical analysis of paraffin-embedded Human Lung Cancer Tissue labeling Smad4 with ab191026 at 1 µg/ml.

  • Immunohistochemical analysis of paraffin-embedded Rat Intestine Tissue labeling Smad4 with ab191026 at 1 µg/ml.

  • Immunohistochemical analysis of paraffin-embedded Rat Intestine Tissue labeling Smad4 with ab191026 at 1 µg/ml.


This product has been referenced in:

  • Feng M  et al. MicroRNA-210 aggravates hypoxia-induced injury in cardiomyocyte H9c2 cells by targeting CXCR4. Biomed Pharmacother 102:981-987 (2018). WB . Read more (PubMed: 29710553) »
  • Feng Y  et al. Alpha-1-antitrypsin functions as a protective factor in preeclampsia through activating Smad2 and inhibitor of DNA binding 4. Oncotarget 8:113002-113012 (2017). Read more (PubMed: 29348884) »
See all 2 Publications for this product

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