Sprouty Homolog 4 (Drosophila) Proteine (SPRY4)

Human Sprouty Homolog 4 (Drosophila) (SPRY4) Interaktionspartner

1. miR181 serves a promoting role in breast cancer at least in part through the inhibition of SPRY4 expression. The present results expand the understanding of the miR181/SPRY4 axis' function during for the malignant progression of breast cancer.

2. The findings indicate that SPRY4 and SPRY4-IT1 may act as oncogenes in testicular germ cell tumors via activation of the PI3K/Akt signaling pathway.

3. Results show that SPRY4 expression level was significantly decreased in glioma tissues, associated with short survival time, and a key target gene of miR-1908.

4. Our data indicate that KMT2C ELs are associated with specific genetic features and that SPRY4 ELs may add prognostic information.

5. Studied BAK1, SPRY4 and GAB2 SNPs in pediatric germ cell tumors(GCT); found a variant in SPRY4 was associated with reduced risk of GCT; a variant in BAK1 was positively associated with GCT with a strong estimated effect for testis tumors; and a SNP in GAB2 was associated with increased risk for GCT.

6. results found that histone methylation mediated by CCAT1 could also contribute to the lower expression of SPRY4 in esophageal squamous cell carcinoma

7. mechanistic evidence that KSRP promotes the down-regulation of Spry4 by a previously unidentified mechanism, i.e. post-transcriptional mRNA regulation.

8. Polymorphisms of KITLG, SPRY4, and BAK1 genes in patients with testicular germ cell tumors and individuals with infertility associated with AZFc deletion of the Y chromosome

9. SPRY4 is involved in the development and progression of colorectal cancer.

10. Small interfering RNA (siRNA)-mediated knockdown of SPRY4 attenuated the AREG-induced down-regulation of E-cadherin.

11. These findings suggest that SPRY4-IT1 plays a direct role in the regulation of metastasis and progression of osteosarcoma.

12. Results identify the tumor suppressor SPRY4 as a novel molecular effector of MT1-MMP affecting melanoma cell motility.

13. Data show that proto-oncogene protein B-raf (BRAF) inhibition induces c-Jun N-terminal kinase (c-JUN) expression and c-JUN abundance and activation by down-regulating SPRY2/4 protein expression.

14. Specific protein 1 plays a crucial role in the regulation of Sprouty4 in response to serum.

15. ZNF703 was a target of SPRY4-IT1.

16. SPRY4 is often deleted in secondary acute myeloid leukemia.

17. Sprouty 2 protein, but not Sprouty 4, is an independent prognostic biomarker for human epithelial ovarian cancer.

18. these results suggest the possibility that SPRY4-IT1 knockdown may induce apoptosis via lipin 2-mediated alterations in lipid metabolism leading to cellular lipotoxicity.

19. SPRY4 may function as a tumor suppressor in endometrial adenocarcinoma.

20. Downregulation of Dusp6, Sprouty4, and Sef--negative modulators of FGF2/ERK1/2 signaling--was present in eutopic endometria of adenomyosis, which may play critical roles in the development of adenomyosis.

Mouse (Murine) Sprouty Homolog 4 (Drosophila) (SPRY4) Interaktionspartner

1. A Sprouty4 reporter to monitor FGF/ERK signaling activity in ESCs and mice.

2. Irf6 and RTK signaling interact in regulating periderm differentiation and function, as well as provide a rationale to screen for epistatic interactions between variants in IRF6 and RTK signaling pathway genes in human orofacial clefting populations.

3. In the present study, it is demonstrated that Spry2 and -4 participate in KA induced neurodegeneration possibly through inhibition of ERK signaling.

4. Autoregulatory loop between TGF-beta1/miR-411-5p/SPRY4 and p38 MAPK pathway in rhabdomyosarcoma modulates proliferation and differentiation.

5. in embryos with lower Spry2;Spry4 gene dosages, we observed a non-fusion of original R2 and M1 Shh signaling domains with consequent formation of a supernumerary tooth primordium from the isolated R2 bud

6. We demonstrate that in spry4-/- mice inflammatory responses, such TNFalpha secretion and macrophage/neutrophil invasion into the lesion site are reduced. In addition, astrocytic gliosis is attenuated and neuronal survival is increased.

7. SPRY4 is a tumor suppressor at 5q whose disruption contributes to a lethal acute myeloid leukemia subtype.

8. In vivo analysis revealed that Spry4 regulated integrin beta3 levels in murine embryos and yolk sacs.

9. We propose that Sprouty genes(Spry2 and Spry4) were implicated during evolution in reduction of the cheek teeth in Muridae, and their deletion can reveal ancestral stages of murine dental evolution.

10. ISG15 mRNA expression and IFN-dependent antiviral responses are enhanced in Spry1,2,4 triple knock-out mouse embryonic fibroblasts, consistent with negative feedback regulatory roles for Spry proteins in IFN-mediated signaling.

11. our results imply that Sprouty2 and -4 are downregulated in the hippocampus during postnatal brain development and that they can act as regulators of developmental axon growth.

12. Interestingly, changes in sprouty gene dosage led to a graded change in incisor number, with progressive decreases in sprouty dosage leading to increasing numbers of teeth.

13. Spry4 and Tpbg/5T4 were detected in Kit-immunoreactive cells only in Kit(K641E), but not in Kit(WT/WT) animals.

14. Spry4, an intracellular FGF receptor antagonist, was expressed in epithelial cells of the fetal lung under control of a doxycycline-inducible system.

15. suggest both redundant and non-redundant functions for Sprouty2 and Sprouty4 on embryonic development and FGF signaling

16. Transgenic expression of murine Spry4 during beta-cell carcinogenesis does not significantly affect tumor outgrowth and progression to tumor malignancy.

17. These data suggest that Sproutys are physiologically important negative regulators of angiogenesis in vivo and novel therapeutic targets for treating peripheral ischemic diseases.

18. Periodic expression of Sprouty4 is controlled by the Notch segmentation clock and may work as a mediator that links the temporal periodicity of clock gene oscillations with the spatial periodicity of boundary formation.

19. Sprouty4 deficiency potentiates Ras-independent angiogenic signals and tumor growth.