Mouse Forkhead box protein E3 (FOXE3) ELISA kit; FKHL12; FREAC8; forkhead; drosophila; homolog-like 12; forkhead box E3

For Research Use Only. Not for use in diagnostic procedures.

Store all reagents at 2-8 degree C

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Small volumes of FOXE3 elisa kit 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.

MBS9331382 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the forkhead box E3 (FOXE3) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing FOXE3. The ELISA analytical biochemical technique of the MBS9331382 kit is based on FOXE3 antibody-FOXE3 antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect FOXE3 antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, FOXE3. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

30,541 Da

forkhead box E3

forkhead box protein E3; dysgenetic lens; Rinshoken cataract

Forkhead box protein E3

FOXE3_MOUSE

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

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