FZD4 sirna

FZD4 siRNA (Mouse)

Cat. Num. AAA8223792

• Gene Names: Fzd4; Fz4
• Reactivity: Mouse
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: FZD4; FZD4 siRNA (Mouse); Frizzled-4; Fz-4; mFz4; CD antigen CD344; FZD4 sirna

• Host: Synthetic
• Reactivity: Mouse
• Specificity: FZD4 siRNA (Mouse) 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: 537

• Applicable Applications for FZD4 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 mouse FZD4 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 FZD4 sirna

siRNA to inhibit FZD4 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 188035913
• NCBI GeneID: 14366
• NCBI Accession #: NP_032081.3
• NCBI GenBank Nucleotide #: NM_008055.4
• UniProt Accession #: Q61088
• Molecular Weight: 60,143 Da
• NCBI Official Full Name: frizzled-4
• NCBI Official Synonym Full Names: frizzled homolog 4 (Drosophila)
• NCBI Official Symbol: Fzd4
• NCBI Official Synonym Symbols: Fz4
• NCBI Protein Information: frizzled-4
• UniProt Protein Name: Frizzled-4
• UniProt Gene Name: Fzd4
• UniProt Synonym Gene Names: Fz-4; mFz4
• UniProt Entry Name: FZD4_MOUSE

Uniprot Description

FZD4: Receptor for Wnt proteins. Most of frizzled receptors are coupled to the beta-catenin (CTNNB1) canonical signaling pathway, which leads to the activation of disheveled proteins, inhibition of GSK-3 kinase, nuclear accumulation of beta-catenin (CTNNB1) and activation of Wnt target genes. Plays a critical role in retinal vascularization by acting as a receptor for Wnt proteins and norrin (NDP). In retina, it can be both activated by Wnt protein-binding, but also by a Wnt-independent signaling via binding of norrin (NDP), promoting in both cases beta-catenin (CTNNB1) accumulation and stimulation of LEF/TCF-mediated transcriptional programs. A second signaling pathway involving PKC and calcium fluxes has been seen for some family members, but it is not yet clear if it represents a distinct pathway or if it can be integrated in the canonical pathway, as PKC seems to be required for Wnt-mediated inactivation of GSK-3 kinase. Both pathways seem to involve interactions with G-proteins. May be involved in transduction and intercellular transmission of polarity information during tissue morphogenesis and/or in differentiated tissues. Defects in FZD4 are the cause of vitreoretinopathy exudative type 1 (EVR1); also known as autosomal dominant familial exudative vitreoretinopathy (FEVR) or Criswick- Schepens syndrome. EVR1 is a disorder of the retinal vasculature characterized by an abrupt cessation of growth of peripheral capillaries, leading to an avascular peripheral retina. This may lead to compensatory retinal neovascularization, which is thought to be induced by hypoxia from the initial avascular insult. New vessels are prone to leakage and rupture causing exudates and bleeding, followed by scarring, retinal detachment and blindness. Clinical features can be highly variable, even within the same family. Patients with mild forms of the disease are asymptomatic, and their only disease-related abnormality is an arc of avascular retina in the extreme temporal periphery. Belongs to the G-protein coupled receptor Fz/Smo family.

Protein type: Membrane protein, multi-pass; Membrane protein, integral; Receptor, GPCR; GPCR, Fz/Smo family

Cellular Component: cell surface; membrane; plasma membrane; integral to membrane; intercellular junction

Molecular Function: G-protein coupled receptor activity; Wnt-protein binding; protein binding; Wnt receptor activity; signal transducer activity; transmembrane receptor activity; protein homodimerization activity; protein heterodimerization activity; ubiquitin protein ligase binding; cytokine binding; PDZ domain binding

Biological Process: positive regulation of JNK activity; blood vessel development; Wnt receptor signaling pathway; multicellular organismal development; positive regulation of transcription, DNA-dependent; Wnt receptor signaling pathway through beta-catenin; signal transduction; progesterone secretion; locomotion during locomotory behavior; G-protein coupled receptor protein signaling pathway; Wnt receptor signaling pathway, calcium modulating pathway; cell surface receptor linked signal transduction; sensory perception of sound; regulation of vascular endothelial growth factor receptor signaling pathway; luteinization; positive regulation of transcription factor activity; vasculogenesis