Overview

  • Product nameHuman FOXE3 peptide

Description

  • NatureSynthetic
  • Amino Acid Sequence
    • SpeciesHuman
    • SequenceAGRSDMDPPAAFS-C
    • Amino acids2 to 14

Specifications

Our Abpromise guarantee covers the use of ab23063 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

  • Applications

    Blocking

  • FormLiquid
  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.

General Info

  • Alternative names
    • Drosphilia Forkhead Homolog Like 12
    • FKHL 12
    • FKHL12
    • Forkhead Box E3
    • Forkhead box protein E3
    • Forkhead Related Activator 8
    • Forkhead related protein FKHL12
    • Forkhead-related protein FKHL12
    • Forkhead-related transcription factor 8
    • Foxe3
    • FOXE3 forkhead box E3
    • FOXE3_HUMAN
    • FREAC 8
    • FREAC-8
    • FREAC8
    see all
  • 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

References for Human FOXE3 peptide (ab23063)

ab23063 has not yet been referenced specifically in any publications.

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