Fzd4 (NM_008055) Mouse Tagged ORF Clone Lentiviral Particle

SKU MR208593L3V

Lenti ORF particles, Fzd4 (Myc-DDK-tagged) - Mouse frizzled homolog 4 (Drosophila) (Fzd4), 200ul, >10^7 TU/mL

Product Data

• Type: Mouse Tagged ORF Clone Lentiviral Particle
• Tag: Myc-DDK
• Target Symbol: Fzd4
• Synonyms: Fz4
• Vector: pLenti-C-Myc-DDK-P2A-Puro
• Mammalian Cell Selection: Puromycin
• Sequence Data:
  ORF Nucleotide Sequence

  The ORF insert of this clone is exactly the same as(MR208593).
• ACCN: NM_008055
• ORF Size: 1611 bp
• OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info
• OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene.
• Shipping: Dry Ice

Reference Data

• RefSeq: NM_008055.2, NP_032081.2
• RefSeq Size: 3685 bp
• RefSeq ORF: 1614 bp
• Locus ID: 14366
• UniProt ID: Q61088
• Cytogenetics: 7 49.32 cM
• Summary: 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. Activation by Wnt5A stimulates PKC activity via a G-protein-dependent mechanism.[UniProtKB/Swiss-Prot Function]