FOXE3 sirna

FOXE3 siRNA (Human)

Cat. Num. AAA8228932

• Gene Names: FOXE3; FKHL12; FREAC8
• Reactivity: Human
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: FOXE3; FOXE3 siRNA (Human); FKHL12; FREAC8; Forkhead box protein E3; Forkhead-related protein FKHL12; Forkhead-related transcription factor 8; FREAC-8; FOXE3 sirna

• Host: Synthetic
• Reactivity: Human
• Specificity: FOXE3 siRNA (Human) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 319

• Applicable Applications for FOXE3 sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of human FOXE3 gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for FOXE3 sirna

siRNA to inhibit FOXE3 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 11386197
• NCBI GeneID: 2301
• NCBI Accession #: NP_036318.1
• NCBI GenBank Nucleotide #: NM_012186.2
• UniProt Accession #: Q13461; Q5SVY9; Q9NQV9
• Molecular Weight: 33,234 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: FKHL12; FREAC8
• NCBI Protein Information: forkhead box protein E3
• UniProt Protein Name: Forkhead box protein E3
• Protein Family: Forkhead box protein
• UniProt Gene Name: FOXE3
• UniProt Synonym Gene Names: FKHL12; FREAC8; FREAC-8
• UniProt Entry Name: FOXE3_HUMAN

NCBI Description

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 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

Chromosomal Location of Human Ortholog: 1p32

Cellular Component: transcription factor complex; nucleus

Molecular Function: 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; cell development; positive regulation of epithelial cell proliferation

Disease: Anterior Segment Mesenchymal Dysgenesis; Aphakia, Congenital Primary