anti-Dishevelled, Dsh Homolog 3 (Drosophila) (DVL3) Antikörper

Xenopus laevis Dishevelled, Dsh Homolog 3 (Drosophila) (DVL3) Interaktionspartner

1. Different Dvl proteins (Dvl1, Dvl2, Dvl3) and the composition of dishevelled-beta-arrestin protein complexes contribute to the specific activation of individual branches of Wnt signaling in Xenopus gastrulation.

2. Data show that maternal Dvl2 and 3 are required for convergence extension movements downstream of the dorsally localized signaling pathway activated by Xnr3, but not downstream of the pathway activated by activin.

Mouse (Murine) Dishevelled, Dsh Homolog 3 (Drosophila) (DVL3) Interaktionspartner

1. Dvl-2 and Dvl-3 have a widespread distribution in both the olfactory epithelium and olfactory bulb

2. Dvl3 is important for IPMK to access substrates and generate IP5, activating down-stream signaling.

3. Dishevelled-KSRP complex operates in Wnt regulation of beta-catenin, functioning post-transcriptionally upon CTNNB1 mRNA stability.

4. Dvl2 and Dvl3 proteins were found to be localized to the apical side of the node cells, and their location was polarized to the posterior side of the cells before the posterior positioning of the basal body.

5. As embryos reach blastocyst stage, Dishevelled 2 becomes increasingly associated with cell membrane in trophectoderm cells, while at E4.5, Dishevelled 3 is highly enriched in the cytoplasm of inner cell mass cells.

6. The expression of Dishevelleds in mammalian cells provide an estimate of the relative cellular abundance of each Dvl.

7. G alpha o mediates WNT-JNK signaling through dishevelled 1 and 3, RhoA family members, and MEKK 1 and 4 in mammalian cells

8. Dvl1, Dvl2 and Dvl3 are functionally redundant in cardiac outflow tract, cochlea, and neural tube development.

Human Dishevelled, Dsh Homolog 3 (Drosophila) (DVL3) Interaktionspartner

1. In silico modeling and in vitro biophysical methods explain how CK1epsilon-specific phosphorylation events control conformational dynamics of DVL3 in living cells upon Wnt pathway stimulation via modulation of the PDZ domain and its interaction with DVL3 C-terminus.

2. downregulation of ASPM expression pronouncedly attenuated the proliferation, colony formation, and the invasive behavior of PCA cells, and dramatically reduced the number of ALDH(+) CSCs and inhibited cancer stemness and tumorigenicity. Mechanistically, ASPM interacts with disheveled-3 (Dvl-3), a cardinal upstream regulator of canonical Wnt signaling, and inhibits its proteasome-dependent degradation

3. These findings expand the clinical spectrum of Robinow syndrome associated with DVL3 mutations. To date, comparison of clinical data of DVL3 mutation-positive individuals with those of patients with genetically different forms did not allow delineation of gene-specific phenotypes.

4. Dvl3 is overexpressed in human HCCs. The NP-Dvl3 is the more stable and active form of the protein and enhances HCC stemness.

5. we found that Wnt3a treatment rapidly induces hyperphosphorylation and stabilization of Dvl2 and Dvl3. Our findings suggest a model of positive regulation of PKCzeta-mediated Dvl signaling activity, to produce a strong and sustained response to Wnt3a treatment by stabilizing Dvl protein levels.

6. Studied and identified candidate biomarkers of biochemical recurrence (BCR) of prostate adenocarcinoma by integrating reverse-phase protein array (RPPA) and mRNA datafrom The Cancer Genome Atlas (TCGA). Found DVL3 was expressed in patients with a higher risk of BCR. DVL3 may be a novel and easily applicable recurrence predictor of localised prostate adenocarcinoma.

7. two mutually exclusive functions of the DEP domain in Wnt signal transduction - binding to Frizzled to recruit Dishevelled to the receptor complex, is reported.

8. Genetic changes between MLH1 and MSH2 were significantly positively correlated (p = 0.032). We also noted a positive correlation between genetic changes of MSH2 and DVL3 genes (p = 0.034).

9. Data show that dishevelled proteins DVL1, 2 and 3 were exclusively expressed in chronic lymphatic leukaemia (CLL) cells as compared to normal peripheral blood mononuclear cells (PBMCs).

10. Kif26b, together with Dvl3/Daam1, initiates cell polarity through the control of planar cell polarity-signaling pathway-dependent activation in endothelial cells.

11. DVL3 transcripts decreased in individuals with major depressive disorder

12. we demonstrate that normally ALFY attenuates the canonical Wnt signaling pathway via autophagy-dependent removal specifically of aggregates of DVL3 and not of Dvl1 or Dvl2.

13. All variants in DVL3 result in a -1 frameshift, indicating that these highly specific alterations might be a common cause of dominant Robinow syndrome.

14. data suggest that miR-204-5p regulates adipogenesis by controlling DVL3 expression and subsequently inhibiting the activation of the Wnt/beta-catenin signaling pathway.

15. findings confirm that p38 and PAX2 are important for the Dvl-3 induced upregulation of p120ctn

16. Tumors that responded to IGFIR inhibition contain relatively lower levels of DVL3 protein than resistant tumors.

17. data (i) support previous the assumption that CK1 acts via phosphorylation of distinct residues as the activator as well as the shut-off signal of Wnt/beta-catenin signaling and (ii) suggest that CK1 acts on Dvl via different mechanism than Fzd5.

18. High expression of IGFBP7 in fibroblasts induced by colorectal cancer cells is co-regulated by TGF-beta and Wnt signaling in a Smad2/3-Dvl2/3-dependent manner.

19. Study showed an association of DVL-1 and DVL-3 with Hirschsprung's disease.

20. AMPK activators suppress cervical cancer cell growth by impairing DVL3 protein synthesis via AMPK/mTOR signaling and/or partially promoting the proteasomal degradation of DVL3

Zebrafish Dishevelled, Dsh Homolog 3 (Drosophila) (DVL3) Interaktionspartner

1. Maternal transcripts for dvl2 and dvl3a are most abundantly expressed, whereas the transcript levels of other dvl genes are negligible. Dvl2 and Dvl3a products are required for the activation of zygotic Wnt/ss-catenin signaling and Wnt/planar cell polarity pathway, and regulate zygotic developmental processes in a dosage-dependent manner.