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Human Rap Guanine Nucleotide Exchange Factor (GEF) 1 (RAPGEF1) interaction partners

1. our studies uncover novel mechanisms by which C3G controls key aspects of tumorigenesis.

2. C3G/RAP1 activity is involved in the metastatic spread of epithelial ovarian cancer.

3. C3G plays an important role in platelet clotting through a mechanism involving its GEF activity and suggest that it might be also involved in neutrophil development.

4. The possibility of cellular phospho-C3G (pC3G) being a substrate of the intracellular T-cell protein tyrosine phosphatase TC-PTP (PTPN2) using the human neuroblastoma cell line, was studied.

5. Lyn controls spatial activation of Rap1 by recruiting the CrkL-C3G protein complex to the leading edge

6. found somatic demethylation of a relaxed-criterion CpG island (CGI-B) located in the first intron of RAPGEF1 in 40% of colon cancers and 8% of gastric cancers relative to their matching normal tissues that were always methylated

7. Data demonstrated that the polymorphism in TP53 (rs1042522) was associated with type 2 diabetes, and that potential interaction of TP53 (rs1042522) and RAPGEF1 (rs11243444), or NRF1 (rs1882095) increased the risk of type 2 diabetes.

8. significant positive correlation between layers II and IV of the dorso-lateral prefrontal cortex in the percentage of MR-GEF expressing neurons in individuals with bipolar disorder

9. C3G overexpression induces neurite-like extensions in MDA-MB-231 and BT549 breast carcinoma cells and not in a variety of other cancer cell lines examined.

10. C3G as a novel target of c-Abl

11. ALK activation of Rap1 via the Rap1-specific GEF C3Gmay contribute to cell proliferation and oncogenesis of neuroblastoma.

12. Cbl-b plays a negative role in Crk-L-C3G-mediated Rap1 and LFA-1 activation in T cells.

13. C3G and Hck interact physically and functionally in vivo to activate kinase-dependent and caspase-mediated apoptosis, which is independent of catalytic domain of C3G

14. C3G interferes with at least two separate aspects of oncogenic transformation - cell cycle progression and loss of contact inhibition.

15. amplification and increased expression of the C3G gene may play some role in human lung carcinogenesis through derangement of the CRK-Rap1 signaling pathway

16. Src family kinases or pervanadate treatment induces phosphorylation of C3G on Y504. Unlike C3G, which is mostly cytosolic, pY504C3G locates to the Golgi & subcortical actin cytoskeleton, providing evidence for a function for C3G at these compartments.

17. Inactivation of Crk SH3 domain-binding guanine nucleotide-releasing factor is associated with cervical squamous cell carcinoma

18. C3G triggers PP2A activation and binding to MEK and ERK at the subcortical actin cytoskeleton, thus favouring ERK dephosphorylation.

19. Results identify a mechanism by which the WAVE2 complex regulates T cell receptor signaling to Rap1 and integrin activation via Abl- and CrkL-C3G.

20. Rap1 and its exchange factor C3G in mediating Fc gammaR-dependent phagocytosis.

Mouse (Murine) Rap Guanine Nucleotide Exchange Factor (GEF) 1 (RAPGEF1) interaction partners

1. C3G is required in cortical neurons for both the specification of an axon and the initiation of radial migration by forming a leading process.

2. results provide evidence that C3G plays an important role in myogenic differentiation by coordinating cell cycle exit, actin dynamics and survival signaling.

3. C3G regulates sympathetic preganglionic neuron migration by acting downstream in the reelin signaling pathway.

4. Data indicate that chemical rescue of c-Src provided a tool to dissect the spatiotemporal mechanism of activation of the Rap1 guanine exchange factor, C3G, one of the identified potential c-Src substrates that plays a role in focal adhesion signaling.

5. GEF and Dlx1/2 form part of a common signalling pathway during GABAergic neuronal development.

6. Guanine nucleotide releasing factor 2 is a negative regulator of Mitogen-Activated Protein Kinase 14 in mouse embryonic fibroblasts and can promote cell survival or cell death depending on the stimuli.

7. Targeted disruption of Ras-Grf2 shows its dispensability for mouse growth and development.

8. These results show that C3G is required for (1) vascular myogenesis, (2) the formation of paxillin- and integrin beta1-positive, but not integrin beta3-positive, cell adhesions and (3) normal response to PDGF, necessary for vascular myogenesis.

9. roles of C3G-Rap1 signaling pathway in various biological processes

10. Our results show that the size of the cortical neural precursor population is controlled by C3G-mediated inhibition of the Ras signalling pathway.

11. C3G regulates cortical neuron migration, preplate splitting and radial glial cell attachment.

Pig (Porcine) Rap Guanine Nucleotide Exchange Factor (GEF) 1 (RAPGEF1) interaction partners

1. the SSC5:60296617 SNP may affect teat number by regulating the interaction of EPS8 and RAPGEF1 and, finally, affecting the mammogenesis of pigs