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Validated All-in-One™ qPCR Primer for FZD4(NM_012193.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene is a member of the frizzled gene family. Members of this family encode seven-transmembrane domain proteins that are receptors for the Wingless type MMTV integration site family of signaling proteins. Most frizzled receptors are coupled to the beta-catenin canonical signaling pathway. This protein may play a role as a positive regulator of the Wingless type MMTV integration site signaling pathway. A transcript variant retaining intronic sequence and encoding a shorter isoform has been described, however, its expression is not supported by other experimental evidence. [provided by RefSeq].
Gene References into function
- Functions in retinal angiogenesis. Mutations disrupts angiogenesis in vitreoretinopathy.
- High-resolution genotyping and haplotype analysis excluded FZD4 as the defective gene in a family previously linked to the EVR1 locus.
- Familial exudative vitreoretinopathy has mutations in a second gene at the EVR1 locus, low-density-lipoprotein receptor-related protein 5 (LRP5), a Wnt coreceptor
- Eight mutations have been identified in the FZD4 gene in a cohort of 40 unrelated patients with FEVR (familial exudative vitreoretinopathy)
- FZD4 mutations are associated with autosomal dominant familial exudative vitreoretinopathy
- A novel missense mutation in the FZD4 gene was identified in Japanese patients with FEVR (familial exudative vitreoretinopathy).
- mutations in the LRP5 and/or FZD4 genes may have roles in familial exudative vitreoretinopathy
- Mutations in FZD4 were observed in 5.6% of studied clinically diagnosed familial exudative vitreoretinopathy in Indian population. Could play vital role in pathogenesis and provide greater insight in to genotype/phenotypic functions of FZD4 gene.
- Fz4 expression may play a critical role in responses to Wnt signaling in the tumor microenvironment.
- sFRP-1 can interact with Wnt receptors Frizzled 4 and 7 on endothelial cells to transduce downstream to cellular machineries requiring Rac-1 activity in cooperation with GSK-3beta
- Homozygous state for the FZD4 gene is possibly involved in the severity of the familial exudative vitreoretinopathy phenotype
- Report activation of Wnt signalling in acute myeloid leukemia by induction of Frizzled-4.
- The clinical features in the three children and their relatives with a documented FZD4 mutation support the previous reports of a high degree of intrafamilial and interfamilial variability in familial exudative vitreoretinopathy (FEVR).