anti-DVL1 (DVL1) Antikörper

Human Dishevelled, Dsh Homolog 1 (Drosophila) (DVL1) Interaktionspartner

1. Lack of DVL prevents NEK2-controlled dissolution of loose centrosomal linker and subsequent centrosomal separation. Increased DVL levels, in contrast, sequester centrosomal NEK2 and mimic monopolar spindle defects induced by a dominant negative version of this kinase.

2. These results identify USP4 as a novel regulator of Dvl in Wnt/beta-catenin signal and show its involvement in Wnt3a-induced osteoblast differentiation

3. Authors conclude that the planar cell polarity (PCP) pathway contributes significantly to the motility and hence the invasiveness of glioblastoma multiforme (GBM) cells, and that Nrdp1 acts as a negative regulator of PCP signaling by inhibiting Dvl through a novel polyubiquitination mechanism.

4. The DEP domain of Dishevelled undergoes a conformational switch, from monomeric to swapped dimer, to trigger DIX domain-dependent polymerization and signaling to beta-catenin.

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

6. we show that Wnt5a rapidly represses rDNA gene transcription in breast cancer cells and generates a chromatin state with reduced transcription of rDNA by RNA polymerase I (Pol I). These effects were specifically dependent on Dishevelled1 (DVL1), which accumulates in nucleolar organizer regions (NORs) and binds to rDNA regions of the chromosome.

7. 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).

8. The secreted frizzled-related protein and disheveled protein family members appear to be actively involved in the pathogenesis of primary testicular germ cell tumors.

9. Data show that receptor for activated C kinase 1 (RACK1) interacts with Dishevelled (Dvl) proteins and promotes their lysosomal degradation, and this effect is enhanced by autophagy induction.

10. TMEM88 stimulated triple negative breast cancer cell invasion by interacting with DVLl.

11. Specific -1 frameshift variants in the penultimate exon of DVL1 cause autosomal-dominant Robinow syndrome.

12. Results show that coexpression of IQGAP1 and Dvl in the cytoplasm and nucleus was correlated with the lymph nodal metastase and poor prognosis of non-small cell lung cancer.

13. Data indicate Dishevelled (DVL) as a dual function adaptor to recruit negative regulators ZNRF3/RNF43 to Wnt receptors to ensure proper control of pathway activity.

14. silencing DVL1 sensitized A2780/Taxol cells to paclitaxel, by down-regulating AKT/GSK-3beta/beta-catenin signalling, providing a novel strategy for chemosensitization of ovarian cancer to paclitaxel-induced cytotoxicity.

15. Mutations in DVL1 cause an osteosclerotic form of Robinow syndrome, with the osteosclerosis possibly the result of an interaction between the wild-type and mutant alleles, leading to elevated canonical Wnt signaling.

16. DVL1 frameshift mutations clustering in the penultimate exon cause autosomal-dominant Robinow syndrome.

17. Authors propose a model for Rac1 activation where SIRT1/2 positively modulates the DVL/TIAM1/Rac1 axis and promotes sustained pathway activation.

18. Dvl overexpression may contribute to the malignant proliferation and invasion of human glioma.

19. DVL is a master regulator of FZD6/G-protein signaling

20. DVL1 was localized in the cytoplasm of CRC cells.

Mouse (Murine) Dishevelled, Dsh Homolog 1 (Drosophila) (DVL1) Interaktionspartner

1. Data show that the peptide binding pocket of the Dishevelled 1 (Dvl1) PDZ domain is stabilized upon CXXC finger 5 protein (CXXC5) binding.

2. Here we show that the peptide-binding pocket of the Dvl PDZ domain can be occupied by Dvl's own highly conserved C-terminus, inducing a closed conformation.

3. The interaction of Dvl1 with Syt-1, which is regulated by Wnts, modulates neurotransmitter release.

4. High disheveled expression is associated with pulmonary fibrosis.

5. findings indicate that Dvl-1 may be an underlying participant of oxidative stress induced by selenium deficiency

6. These results support a novel cell-autonomous postsynaptic role for Dact1, in cooperation with Dishevelled-1 and possibly Disrupted in Schizophrenia-1, in the formation of synapses on cortical interneuron dendrites.

7. we show that Dvl-1 expression is restricted to OSNs in the dorsal recess of the nasal cavity, and labels a unique subpopulation of glomeruli. Dvl-2 and Dvl-3 have a widespread distribution in both the olfactory epithelium and olfactory bulb .

8. Fuzzy appears to control subcellular localization of the core PCP protein Dishevelled, recruiting it to Rab8-positive vesicles and to the basal body and cilium. We show that loss of Fuzzy results in inhibition of PCP signaling

9. A Wnt5a--> Dvl PCP signaling cascade may regulate actin polymerization and protrusive cell behavior in the caudal splanchnic mesoderm to promote second heart field deployment, outflow tract lengthening and cardiac looping.

10. Findings indicate that Daple interacts with Dishevelled to direct the Dishevelled/protein kinase lambda protein complex to activate Rac, which in turn mediates the non-canonical Wnt signalling pathway required for cell migration.

11. The antagonistic functions of Vangl2 and Dvl1 allow sharpening of planar cell polarity signaling locally on the tips of the filopodia to sense directional cues, Wnts, eventually causing turning of growth cones.

12. p114-RhoGEF and Lfc are critically involved in Wnt-3a- and Dvl-induced RhoA activation and neurite retraction in N1E-115 cells.

13. TMEM88 associates with Dvl proteins and regulates Wnt signaling in a context-dependent manner

14. phosphorylation of Dvl triggers negative feedback regulation for different branches of Wnt signaling in a Ror2-dependent manner.

15. Loss of CYLD instigates tumor growth in human cylindromatosis through a mechanism in which hyperubiquitination of polymerized Dvl drives enhancement of Wnt3/beta-catenin responses.

16. preliminary characterization of it's interaction with Smad3

17. Data show that Dishevelled (Dvl) binding peptides of Frizzled inhibited canonical Wnt signaling and blocked Wnt-induced secondary axis formation in a dose-dependent manner, but did not block noncanonical Wnt signaling.

18. The specificity of observed social interaction deficits suggests that lack of Dvl1 is associated with deficits in the recognition of social hierarchy and dominance. The sensorimotor gating deficit was subject to environmental influences.

19. Results suggest that casein kinase Iepsilon functions as a molecular switch to direct Dishevelled (Dvl) from the c-Jun N-terminal kinase pathway to the beta-catenin pathway, possibly by altering the conformation of the C terminus of Dvl.

20. DEP domain is responsible for the membrane translocation of Dvl-1 protein upon Wnt signal stimulation.

Xenopus laevis Dishevelled, Dsh Homolog 1 (Drosophila) (DVL1) 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.