Key features and details
- Rabbit polyclonal to FOXC1
- Suitable for: WB, IHC-P
- Reacts with: Human
- Isotype: IgG
Product nameAnti-FOXC1 antibody
See all FOXC1 primary antibodies
DescriptionRabbit polyclonal to FOXC1
Tested applicationsSuitable for: WB, IHC-Pmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat, Cow, Monkey
- Human colon tissue
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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. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.05% Sodium azide
Constituents: 99% PBS, 0.2% Gelatin
Concentration information loading...
Our Abpromise guarantee covers the use of ab115201 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/250 - 1/1000. Predicted molecular weight: 57 kDa.|
|IHC-P||1/200. 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
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- FKHL 7 antibody
ab115201, at 10 ug/ml, staining FOXC1 in formalin fixed, paraffin embedded Human colon tissue by Immunohistochemistry. After incubation with the primary antibody, slides were incubated with biotinylated goat anti-rabbit IgG secondary antibody, followed by alkaline phosphatase-streptavidin and chromogen.
ab115201 has been referenced in 2 publications.
- Liu Y et al. MicroRNA-200a Affects the Proliferation of Airway Smooth Muscle Cells and Airway Remodeling by Targeting FOXC1 via the PI3K/AKT Signaling Pathway in Ovalbumin-Induced Asthmatic Mice. Cell Physiol Biochem 50:2365-2389 (2018). PubMed: 30423573
- Bin L et al. Forkhead Box C1 Regulates Human Primary Keratinocyte Terminal Differentiation. PLoS One 11:e0167392 (2016). IHC-P ; Human . PubMed: 27907090