- Datasheet
- Specific References (1)
- Protocols
Overview
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Product nameAnti-FOXC1 antibody
See all FOXC1 primary antibodies -
DescriptionRabbit polyclonal to FOXC1
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Tested applicationsSuitable for: WBmore details
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Species reactivity
Predicted to work with: Mouse, Human, Xenopus laevis
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Immunogen
Synthetic peptide conjugated to KLH derived from within residues 500 - 600 of Human FOXC1.
(Peptide available as ab26345.)
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Positive control
- This antibody gave a positive signal in HepG2 Whole Cell Lysate
Properties
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FormLiquid
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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 or -80°C. Avoid freeze / thaw cycle.
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Storage bufferPreservative: 0.02% Sodium Azide
Constituents: 1% BSA, PBS, pH 7.4 -
Concentration information loading... -
PurityImmunogen affinity purified
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ClonalityPolyclonal
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IsotypeIgG
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Research areas
Associated products
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Compatible Secondaries
Applications
Our Abpromise guarantee covers the use of ab24067 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 1 µg/ml. Detects a band of approximately 57 kDa (predicted molecular weight: 57 kDa). |
Target
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FunctionBinding of FREAC-3 and FREAC-4 to their cognate sites results in bending of the DNA at an angle of 80-90 degrees.
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Tissue specificityExpressed in all tissues and cell lines examined.
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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.
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Cellular localizationNucleus.
- Information by UniProt
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Database links
- Entrez Gene: 2296 Human
- Entrez Gene: 17300 Mouse
- GenBank: NP_001444 Human
- Omim: 601090 Human
- SwissProt: Q12948 Human
- SwissProt: Q61572 Mouse
- SwissProt: Q32NP8 Xenopus laevis
- Unigene: 348883 Human
see all -
Alternative names
- ARA antibody
- FKH L7 antibody
- FKHL 7 antibody
see all
Anti-FOXC1 antibody images
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Western blot - FOXC1 antibody (ab24067)Anti-FOXC1 antibody (ab24067) at 1 µg/ml + HepG2 (Human hepatocellular liver carcinoma cell line) Whole Cell Lysate at 10 µg
Secondary
Goat polyclonal to Rabbit IgG - H&L - Pre-Adsorbed (HRP) at 1/3000 dilution
Performed under reducing conditions.
Predicted band size : 57 kDa
Observed band size : 57 kDa
Additional bands at : 110&120 kDa. We are unsure as to the identity of these extra bands.
Protocols
References for Anti-FOXC1 antibody (ab24067)
This product has been referenced in:
- Ito YA et al. Severe molecular defects of a novel FOXC1 W152G mutation result in aniridia. Invest Ophthalmol Vis Sci 50:3573-9 (2009). Read more (PubMed: 19279310) »
Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"