Key features and details
- Goat polyclonal to FOXC1
- Suitable for: WB, ELISA, IHC-P
- Reacts with: Human
- Isotype: IgG
Product nameAnti-FOXC1 antibody
See all FOXC1 primary antibodies
DescriptionGoat polyclonal to FOXC1
Tested applicationsSuitable for: WB, ELISA, IHC-Pmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Xenopus laevis
- Human brain, cerebellum and spleen tissue; Human Bone Marrow lysate.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term.
Storage bufferpH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 99% Tris buffered saline, 0.5% BSA
Concentration information loading...
PurityProtein G purified
Our Abpromise guarantee covers the use of ab117088 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.5 - 1.5 µg/ml. Predicted molecular weight: 57 kDa.|
|IHC-P||Use a concentration of 3.75 µg/ml. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.|
FunctionBinding of FREAC-3 and FREAC-4 to their cognate sites results in bending of the DNA at an angle of 80-90 degrees.
Tissue specificityExpressed in all tissues and cell lines examined.
Involvement in diseaseDefects 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 similaritiesContains 1 fork-head DNA-binding domain.
- Information by UniProt
- ARA antibody
- FKH L7 antibody
- FKHL 7 antibody
Anti-FOXC1 antibody (ab117088) at 0.5 µg/ml + Human bone marrow lysate in RIPA buffer at 35 µg
Developed using the ECL technique.
Predicted band size: 57 kDa
ab117088, at 3.75 µg/ml, staining FOXC1 in Formalin-fixed, Paraffin-embedded Human brain, cerebellum tissue by Immunohistochemistry followed by biotinylated secondary antibody, alkaline phosphatase-streptavidin and chromogen.
ab117088, at 3.75 µg/ml, staining FOXC1 in Formalin-fixed, Paraffin-embedded Human spleen tissue by Immunohistochemistry followed by biotinylated secondary antibody, alkaline phosphatase-streptavidin and chromogen.
ab117088 has not yet been referenced specifically in any publications.