Mouse forkhead box E3 ELISA Kit | FOXE3 elisa kit

Mouse Forkhead box protein E3, FOXE3 ELISA Kit

Cat. Num. AAA9331382

• Gene Names: Foxe3; dyl; rct; FREAC8
• Reactivity: Mouse
• Synonyms: forkhead box E3; Mouse Forkhead box protein E3; FOXE3 ELISA Kit; Mouse Forkhead box protein E3 (FOXE3) ELISA kit; FKHL12; FREAC8; forkhead; drosophila; homolog-like 12; FOXE3 elisa kit

• Reactivity: Mouse

• Preparation and Storage: Store all reagents at 2-8 degree C

NCBI and Uniprot Product Information

• NCBI GI #: 7657098
• NCBI GeneID: 30923
• NCBI Accession #: NP_056573.1
• NCBI GenBank Nucleotide #: NM_015758.2
• UniProt Accession #: Q9QY14
• Molecular Weight: 30,541 Da
• NCBI Official Full Name: forkhead box protein E3
• NCBI Official Synonym Full Names: forkhead box E3
• NCBI Official Symbol: Foxe3
• NCBI Official Synonym Symbols: dyl; rct; FREAC8
• NCBI Protein Information: forkhead box protein E3; dysgenetic lens; Rinshoken cataract
• UniProt Protein Name: Forkhead box protein E3
• Protein Family: Forkhead box protein
• UniProt Gene Name: Foxe3
• UniProt Entry Name: FOXE3_MOUSE

Uniprot Description

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

Cellular Component: transcription factor complex; nucleus

Molecular Function: DNA binding; sequence-specific DNA binding; transcription factor activity

Biological Process: transcription from RNA polymerase II promoter; regulation of transcription from RNA polymerase II promoter; camera-type eye development; transcription, DNA-dependent; eye development; regulation of transcription, DNA-dependent; cell development; positive regulation of epithelial cell proliferation