Full Product Name
FOXE3 antibody - C-terminal region
Product Gene Name
anti-FOXE3 antibody
[Similar Products]
Product Synonym Gene Name
FKHL12; FREAC8[Similar Products]
Antibody/Peptide Pairs
FOXE3 peptide (MBS3225892) is used for blocking the activity of FOXE3 antibody (MBS3200853)
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
Immunogen Sequence
Synthetic peptide located within the following region: PEPPCCAAPD AAAAAFPPCA AAASPPLYSQ VPDRLVLPAT RPGPGPLPAE
3D Structure
ModBase 3D Structure for Q13461
Purity/Purification
Affinity Purified
Form/Format
Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Immunogen
The immunogen is a synthetic peptide directed towards the C terminal region of human FOXE3
Preparation and Storage
For short term use, store at 2-8 degree C up to 1 week. For long term storage, store at -20 degree C in small aliquots to prevent freeze-thaw cycles.
Other Notes
Small volumes of anti-FOXE3 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.
Related Product Information for
anti-FOXE3 antibody
This is a rabbit polyclonal antibody against FOXE3. It was validated on Western Blot and immunohistochemistry
Target Description: Forkhead Box Protein E3 (FOXE3, forkhead-related protein FKHL12, forkhead-related transcription factor 8) is a forkhead/winged helix transcription factor, which is expressed in the developing lens from the start of lens placode induction and becomes restricted to the anterior proliferating cells when lens fiber differentiation begins.
Product Categories/Family for anti-FOXE3 antibody
Polyclonal; Transcription Factor; Transcription Regulation; Various; E3 & Ubiquitin; Immunohistochemistry; Transcription Factors;
Applications Tested/Suitable for anti-FOXE3 antibody
Immunohistochemistry (IHC), Western Blot (WB)
Immunohistochemistry (IHC) of anti-FOXE3 antibody
Human Muscle

Immunohistochemistry (IHC) of anti-FOXE3 antibody
Human Spermatophore

Western Blot (WB) of anti-FOXE3 antibody
WB Suggested Anti-FOXE3 Antibody Titration: 0.2-1 ug/ml
Positive Control: HepG2 cell lysate

NCBI/Uniprot data below describe general gene information for FOXE3. It may not necessarily be applicable to this product.
NCBI Accession #
NP_036318
[Other Products]
NCBI GenBank Nucleotide #
NM_012186
[Other Products]
UniProt Primary Accession #
Q13461
[Other Products]
UniProt Related Accession #
Q13461[Other Products]
NCBI Official Full Name
forkhead box protein E3
NCBI Official Synonym Full Names
forkhead box E3
NCBI Official Symbol
FOXE3 [Similar Products]
NCBI Official Synonym Symbols
AAT11; ASGD2; FKHL12; FREAC8; CTRCT34
[Similar Products]
NCBI Protein Information
forkhead box protein E3
UniProt Protein Name
Forkhead box protein E3
UniProt Synonym Protein Names
Forkhead-related protein FKHL12; Forkhead-related transcription factor 8
Protein Family
Forkhead box protein
UniProt Gene Name
FOXE3 [Similar Products]
UniProt Synonym Gene Names
FKHL12; FREAC8; FREAC-8 [Similar Products]
UniProt Entry Name
FOXE3_HUMAN
NCBI Summary for FOXE3
This intronless gene belongs to the forkhead family of transcription factors, which is characterized by a distinct forkhead domain. The protein encoded functions as a lens-specific transcription factor and plays an important role in vertebrate lens formation. Mutations in this gene are associated with anterior segment mesenchymal dysgenesis and congenital primary aphakia. [provided by RefSeq, Dec 2009]
UniProt Comments for FOXE3
FOXE3: Defects in FOXE3 are a cause of anterior segment mesenchymal dysgenesis (ASMD); 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). 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.
Protein type: DNA-binding
Chromosomal Location of Human Ortholog: 1p32
Cellular Component: transcription factor complex; nucleus
Molecular Function: sequence-specific DNA binding; transcription factor activity
Biological Process: regulation of transcription from RNA polymerase II promoter; transcription from RNA polymerase II promoter; camera-type eye development; cell development; positive regulation of epithelial cell proliferation
Disease: Anterior Segment Mesenchymal Dysgenesis; Aphakia, Congenital Primary
Research Articles on FOXE3
1. The sclerocornea-microphthalmia-aphakia complex is a severe malformative ocular phenotype resulting from mutations in the FOXE3 transcription factor. To date, patients from at least 14 families with this uncommon ocular disorder have been described. The identification of 2 novel pathogenic variants in our patients expands the mutational spectrum in FOXE3-related congenital eye disorders.
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