Sprouty Homolog 4 (Drosophila) Proteins (SPRY4)

Human Sprouty Homolog 4 (Drosophila) (SPRY4) interaction partners

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

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

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

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

5. mechanistic evidence that KSRP (show KHSRP Proteins) promotes the down-regulation of Spry4 by a previously unidentified mechanism, i.e. post-transcriptional mRNA regulation.

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

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

8. Small interfering RNA (siRNA)-mediated knockdown of SPRY4 attenuated the AREG (show AREG Proteins)-induced down-regulation of E-cadherin (show CDH1 Proteins).

9. These findings suggest that SPRY4-IT1 (show HAUS3 Proteins) plays a direct role in the regulation of metastasis and progression of osteosarcoma.

10. Results identify the tumor suppressor SPRY4 as a novel molecular effector of MT1-MMP (show MMP14 Proteins) affecting melanoma cell motility.

Mouse (Murine) Sprouty Homolog 4 (Drosophila) (SPRY4) interaction partners

1. A Sprouty4 reporter to monitor FGF/ERK (show EPHB2 Proteins) signaling activity in ESCs (show NR2E3 Proteins) and mice.

2. Irf6 (show IRF6 Proteins) 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 (show IRF6 Proteins) and RTK signaling pathway genes in human orofacial clefting populations.

3. In the present study, it is demonstrated that Spry2 (show SPRY2 Proteins) and -4 participate in KA induced neurodegeneration possibly through inhibition of ERK (show EPHB2 Proteins) signaling.

4. Autoregulatory loop between TGF-beta1 (show TGFB1 Proteins)/miR (show MLXIP Proteins)-411-5p/SPRY4 and p38 MAPK (show MAPK14 Proteins) pathway in rhabdomyosarcoma modulates proliferation and differentiation.

5. in embryos with lower Spry2 (show SPRY2 Proteins);Spry4 gene dosages, we observed a non-fusion of original R2 and M1 Shh (show SHH Proteins) 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 (show TNF Proteins) 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 (show BCL11A Proteins) 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 (show SPRY2 Proteins) 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.