• Product name

  • Description

    Rabbit polyclonal to FOXC1
  • Host species

  • Tested applications

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

    Reacts with: Human
  • Immunogen

    Synthetic peptide within Human FOXC1 aa 275-325. The exact sequence is proprietary. NP_001444.2
    Database link: Q12948

  • Positive control

    • IP: FOXC1 IP in HeLa whole cell lysate. IHC-P: Human breast carcinoma tissue.



Our Abpromise guarantee covers the use of ab245443 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 Use at 2-10 µg/mg of lysate.
IHC-P 1/500 - 1/2000. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.
  • Application notes
    Is unsuitable for WB.
  • Target

    • Function

      Binding of FREAC-3 and FREAC-4 to their cognate sites results in bending of the DNA at an angle of 80-90 degrees.
    • Tissue specificity

      Expressed in all tissues and cell lines examined.
    • Involvement in disease

      Defects in FOXC1 are the cause of Axenfeld-Rieger syndrome type 3 (RIEG3) [MIM:602482]; also known as Axenfeld-Rieger syndrome (ARS) or Axenfeld syndrome or Axenfeld anomaly. It is characterized by posterior corneal embryotoxon, prominent Schwalbe line and iris adhesion to the Schwalbe line. Other features may be hypertelorism (wide spacing of the eyes), hypoplasia of the malar bones, congenital absence of some teeth and mental retardation. When associated with tooth anomalies, the disorder is known as Rieger syndrome. Glaucoma is a progressive blinding condition that occurs in approximately half of patients with Axenfeld-Rieger malformations.
      Defects in FOXC1 are the cause of iridogoniodysgenesis anomaly (IGDA) [MIM:601631]. IGDA is an autosomal dominant phenotype characterized by iris hypoplasia, goniodysgenesis, and juvenile glaucoma.
      Defects in FOXC1 are a cause of Peters anomaly (PAN) [MIM:604229]. Peters anomaly consists of a central corneal leukoma, absence of the posterior corneal stroma and Descemet membrane, and a variable degree of iris and lenticular attachments to the central aspect of the posterior cornea.
    • Sequence similarities

      Contains 1 fork-head DNA-binding domain.
    • Cellular localization

    • Information by UniProt
    • Database links

    • Alternative names

      • ARA antibody
      • FKH L7 antibody
      • FKHL 7 antibody
      • FKHL7 antibody
      • Forkhead (Drosophila) like 7 antibody
      • Forkhead box C1 antibody
      • Forkhead box protein C1 antibody
      • Forkhead drosophila homolog like 7 antibody
      • Forkhead like 7 antibody
      • Forkhead related activator 3 antibody
      • Forkhead related protein FKHL7 antibody
      • Forkhead related transcription factor 3 antibody
      • Forkhead-related protein FKHL7 antibody
      • Forkhead-related transcription factor 3 antibody
      • FOX C1 antibody
      • FOXC 1 antibody
      • Foxc1 antibody
      • FOXC1_HUMAN antibody
      • FREAC 3 antibody
      • FREAC-3 antibody
      • FREAC3 antibody
      • IGDA antibody
      • IHG 1 antibody
      • IHG1 antibody
      • IRID 1 antibody
      • IRID1 antibody
      • Iridogoniodysgenesis type 1 antibody
      • Myeloid factor delta antibody
      see all


    • Formalin-fixed, paraffin-embedded human breast carcinoma tissue stained for FOXC1 with ab245443 at a 1/1000 dilution in immunohistochemical analysis. DAB staining. Counterstained using hematoxylin (blue).

    • FOXC1 was immunoprecipitated from HeLa (Human epithelial cell line from cervix adenocarcinoma) whole cell lysate (1 mg per IP reaction; 20% of IP loaded).

      ab245443 used for IP at 6 µg/mg lysate. For WB another anti-FOXC1 antibody was used at 1 µg/ml.

      Lane 1: ab245443 IP in HeLa whole cell lysate.
      Lane 2: Control IgG in HeLa whole cell lysate.
      Chemiluminescence detection: 10 seconds.


    ab245443 has not yet been referenced specifically in any publications.

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