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Maturation of a central brain flight circuit in Drosophila requires Fz2 and Ca2+ signaling.
The heterotrimeric G protein Go functions as a transducer of Wingless-Frizzled 2 signaling in the synapse and Ankyrin 2 as a target of Go signaling required for neuromuscular junction formation
Study finds that C-terminal fragments of the Wg receptor DFz2 accumulate in nuclear foci in association with large RNA granules localizing to the space between the inner & and outer nuclear membranes; granules are found at of inner membrane invaginations, are bounded by LamC, and can be seen leaving the nucleus.
Knockdown of Tc-fz1 alone interfered with the formation of the proximo-distal and the dorso-ventral axes during leg development, whereas no effect was observed with single Tc-fz2 or Tc-fz4 RNAi knockdowns.
Wnt-activated growth of the postsynaptic membrane is mediated by the synapse-to-nucleus translocation and active nuclear import of Fz2-C via a selective Importin-beta11/alpha2 pathway.
subcellular Fz localization, through the association with other membrane proteins, is a critical aspect in regulating the signaling specificity within the Wnt/Fz signaling pathways
Frizzled2 achieves ligand capture and internalization, whereas Arrow, and perhaps downstream signalling, are essential for lysosomal targeting.
concluded that, at synapses, Wingless signal transduction occurs through the nuclear localization of DFrizzled2-C for potential transcriptional regulation of synapse development
DFz2 functions as an endocytic receptor for Wingless in the Drosophila wing
Data show that GRIP is necessary for the trafficking of Frizzled-2 to the nucleus.
fzd2 are broadly expressed throughout the head, during zebrafish craniofacial development
frizzled 8c is a receptor for wnt8
conserved role of a Wnt5/Fz2 signaling pathway in islet formation during pancreatic development.
Down-regulation of miR-30a-3p/5p promotes esophageal squamous cell carcinoma cell proliferation by activating the Wnt signaling pathway through inhibition of Wnt2 and Fzd2.
this study presents the crystal structure of a TcdB fragment in complex with the cysteine-rich domain of human FZD2 at 2.5-angstrom resolution, which reveals an endogenous FZD-bound fatty acid acting as a co-receptor for TcdB binding.
our study suggests a role for FZD2 in high-risk neuroblastoma cell growth
Treatment of the cell lines with Fzd2 siRNA resulted in significantly reduced migration and invasiveness but did not affect proliferation.Patients with high Fzd2 expression had significantly poorer recurrencefree survival than those with low expression
Fzd2 did not influence the proliferation of EC cells.
FZD2 was downregulated in an adenoid cystic carcinoma cell line with high metastatic potential, vs another with low potential. Knockdown of FZD2 downregulated the expression of PAI-1.
Sonazoid enhanced sonoporation of the cells with the diagnostic US device and the suppression of proliferation of both HCC cell lines by shRNA-Fz2.
the present study demonstrated that Fzd2 contributes to the migration and invasion of OSCC cells, at least partly through regulation of the STAT3 pathway
CD82 enhanced the expression of miR-203 and directly downregulated FZD2 expression, suppressing cancer metastasis/cell migration by inhibiting the Wnt signaling pathway.
the FRIZZLED2 mutation is a de novo, novel cause for autosomal dominant omodysplasia.
Fz2 was positive in both the cell membrane and cytoplasm of gastric cancer tissues of moderately differentiated and poorly differentiated adenocarcinoma.Fz2 expression pattern in normal stomach tissues.
It is associated with poor prognosis in glioblastoma patients.
Pharmacologic and genetic perturbations reveal that Fzd2 drives epithelial-mesenchymal transition and cell migration through a previously unrecognized, noncanonical pathway that includes Fyn and Stat3.
Data suggest that an anti-Wnt5a antibody was capable of suppressing Wnt5a-dependent internalization of Fz2 receptor, resulting in the prevention of metastasis of gastric cancer cells by inhibiting the activation of Rac1 and the expression of laminin gamma2.
altered expression of FZD2 might be associated with a proliferative status, thus playing a role in the biology of human medulloblastomas
Wnt5a activated Rac in the beta-catenin-independent pathway, and Frizzled2 (Fz2) and Ror1 or Ror2 were required for this action.
Ror2 positively modulates Wnt3a-activated canonical signaling in a lung carcinoma, H441 cell line. This activity of Ror2 is dependent on cooperative interactions with Fzd2 but not Fzd7.
Human Frizzled-2 does not couple to calcium-mediated signaling through Wnt-5 protein and has slowly accumulated in canonical signaling by Wnt-3 protein.
the Wnt5a/Frizzled-2 axis suppresses beta-catenin signaling in hepatocytes in an autocrine manner, thereby contributing to timely conclusion of the liver regeneration process
Fzd2 promotes changes in epithelial cell length and shape. These changes in cell morphology deform the developing lung epithelial tube to generate and maintain new domain branches.
Results provide further insight into the role of Wnt5a and Fzd2 in the pathogenesis of adult amyotrophic lateral sclerosis transgenic mice.
observed genetic interactions between Fz2 and Fz7 and five canonical and/or non-canonical signaling molecules: Dvl3, Wnt3a, Wnt11, Vangl2, and Wnt5a.
Frizzled signaling is involved in diverse tissue closure processes, defects in which account for some of the most common congenital anomalies.
Indicate that myofibroblast migration and differentiation are modulated via Wnt/Fzd signalling.
Protein kinase G is a critical downstream effector of the noncanonical Wnt-Frizzled-2/cGMP/Ca2+ pathway
Preferential expression of Frizzled2 gene is detected in fetal liver kinase (Flk)1-negative and Flk1-positive cells under different culture conditions.
This intronless 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. This gene encodes a protein that is coupled to the beta-catenin canonical signaling pathway. Competition between the wingless-type MMTV integration site family, member 3A and wingless-type MMTV integration site family, member 5A gene products for binding of this protein is thought to regulate the beta-catenin-dependent and -independent pathways.
, drosophila frizzled 2
, frizzled homolog 8
, frizzled homolog 2 (Drosophila)
, frizzled 2
, frizzled 2, seven transmembrane spanning receptor
, frizzled homolog 2
, Drosophila polarity gene (frizzled) homologue
, Drosophila polarity gene homolog 2