Overview

  • Product nameAnti-FOXE3 antibody
    See all FOXE3 primary antibodies
  • Description
    Rabbit polyclonal to FOXE3
  • Tested applicationsSuitable for: WBmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Mouse, Rat, Pig
  • Immunogen

    Synthetic peptide corresponding to a region within the N terminal amino acids 2-51 (AGRSDMDPPA AFSGFPALPA VAPSGPPPSP LAGAEPGREP EEAAAGRGEA) of Human FOXE3 (NP_036318).

  • Positive control
    • SH-SYSY cell lysate

Properties

Applications

Our Abpromise guarantee covers the use of ab90714 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. Predicted molecular weight: 33 kDa. Good results were obtained when blocked with 5% non-fat dry milk in 0.05% PBS-T.

Target

  • Involvement in diseaseDefects in FOXE3 are a cause of anterior segment mesenchymal dysgenesis (ASMD) [MIM:107250]; also known as anterior segment ocular dysgenesis (ASOD). ASMD consists of a range of developmental defects in structures at the front of the eye, resulting from abnormal migration or differentiation of the neural crest derived mesenchymal cells that give rise to the cornea, iris, and other components of the anterior chamber during eye development. Mature anterior segment anomalies are associated with an increased risk of glaucoma and corneal opacity. Conditions falling within the phenotypic spectrum include aniridia, posterior embryotoxon, Axenfeld anomaly, Reiger anomaly/syndrome, Peters anomaly, and iridogoniodysgenesis.
    Defects in FOXE3 are a cause of congenital primary aphakia (CPA) [MIM:610256]. Aphakia is a rare congenital eye disorder in which the lens is missing. It has been histologically subdivided into primary and secondary forms, in accordance with the severity of defects of the ocular tissues, whose development requires the initial presence of a lens. CPA results from an early developmental arrest, around the 4th-5th week of gestation in humans, that prevents the formation of any lens structure and leads to severe secondary ocular defects, including a complete aplasia of the anterior segment of the eye. In contrast, in secondary aphakic eyes, lens induction has occurred, and the lens vesicle has developed to some degree but finally has progressively resorbed perinatally, leading, therefore, to less-severe ocular defects.
  • Sequence similaritiesContains 1 fork-head DNA-binding domain.
  • Developmental stageExpressed in the lens during embryonic development. Predominantly expressed in the anterior lens epithelium but with some expression posteriorly. Not expressed in brain in embryos.
  • Cellular localizationNucleus.
  • Information by UniProt
  • Database links
  • Alternative names
    • Drosphilia Forkhead Homolog Like 12 antibody
    • FKHL 12 antibody
    • FKHL12 antibody
    • Forkhead Box E3 antibody
    • Forkhead box protein E3 antibody
    • Forkhead Related Activator 8 antibody
    • Forkhead related protein FKHL12 antibody
    • Forkhead-related protein FKHL12 antibody
    • Forkhead-related transcription factor 8 antibody
    • Foxe3 antibody
    • FOXE3 forkhead box E3 antibody
    • FOXE3_HUMAN antibody
    • FREAC 8 antibody
    • FREAC-8 antibody
    • FREAC8 antibody
    see all

Anti-FOXE3 antibody images

  • Anti-FOXE3 antibody (ab90714) at 1 µg/ml (in 5% skim milk / PBS buffer) + SH-SYSY cell lysate at 10 µg

    Secondary
    HRP conjugated anti-Rabbit IgG at 1/50000 dilution

    Predicted band size : 33 kDa

References for Anti-FOXE3 antibody (ab90714)

ab90714 has not yet been referenced specifically in any publications.

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