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Rap guanine nucleotide exchange factor

C3G, Guanine Nucleotide-Releasing Factor 2, c(3)G
This gene encodes a human guanine nucleotide exchange factor. It transduces signals from CRK by binding the SH3 domain of CRK, and activating several members of the Ras family of GTPases. This signaling cascade that may be involved in apoptosis, integrin-mediated signal transduction, and cell transformation. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some variants has not been determined. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Rap1, Crk, Src, V1a, CAN
Papers using C3G antibodies
The WAVE2 complex regulates T cell receptor signaling to integrins via Abl- and CrkL–C3G-mediated activation of Rap1
Billadeau Daniel D. et al., In The Journal of Cell Biology, 2003
... The antibody for Abl (clone 8E9) was purchased from BD Biosciences, and the antibody for C3G (RapGEF1, Clone 3D10) was obtained from Novus Biologicals.
Papers on C3G
Interaction of cyanidin-3-O-glucoside with three proteins.
Gao et al., Jinan, China. In Food Chem, May 2016
We studied the binding of cyanidin-3-O-glucoside (C3G) with bovine serum albumin (BSA), hemoglobin (Hb) and myoglobin (Mb), using multi-spectral techniques and molecular modeling.
Hyperglycemia and Anthocyanin Inhibit Quercetin Metabolism in HepG2 Cells.
Chen et al., Boston, United States. In J Med Food, Jan 2016
HepG2 cells were grown for 3 days in Glu ranging from 5.5 to 50 mmol/L and/or cyanidin-3-glucoside (C3G) ranging from 0 to 25 μmol/L.
Enhancement of Cognitive Functions by Aronia melanocarpa Elliot Through an Intermittent Ultrasonication Extraction Process.
Lee et al., Ch'unch'ŏn, South Korea. In J Med Food, Jan 2016
Comparison of the high-performance liquid chromatography chromatograms of the extracts demonstrates that the intermittent ultrasonication process may improve the cognitive activities of Aronia by eluting higher amounts of cyanidin-3-galactoside (C3G).
Serum properdin consumption as a biomarker of C5 convertase dysregulation in C3 glomerulopathy.
López-Trascasa et al., Madrid, Spain. In Clin Exp Immunol, Jan 2016
Serum P levels were measured in 49 patients with histological and clinical evidence of C3 glomerulopathy (C3G).
Anthocyanins contents in the seed coat of black soybean and their anti-human tyrosinase activity and antioxidative activity.
Hsu et al., Taiwan. In Int J Cosmet Sci, Jan 2016
RESULTS: 80% acetone extract from SCBS obtained the highest total phenol, total flavonoid, and cyanidin-3-O-glucoside (C3G) contents among all the extracts, while the hot water extract showed the lowest antioxidant contents.
The Role of Crk Adaptor Proteins in T-Cell Adhesion and Migration.
Isakov et al., Beersheba, Israel. In Front Immunol, 2014
In addition, they constitutively associate, via their SH3 domain, with effector molecules, such as C3G, that mediate cell adhesion and regulate lymphocyte extravasation and recruitment to sites of inflammation.
Current concepts in C3 glomerulopathy.
John et al., Brisbane, Australia. In Indian J Nephrol, 2014
Complement component 3 glomerulopathy (C3G) is a recently defined entity comprising of dense deposit disease and C3 glomerulonephritis.
C3 glomerulopathy: the genetic and clinical findings in dense deposit disease and C3 glomerulonephritis.
Smith et al., London, United Kingdom. In Semin Thromb Hemost, 2014
C3 glomerulopathy (C3G) defines a group of very rare renal diseases in which dysregulation of the alternative and terminal complement pathways plays a pivotal pathogenic role.
Treatment of C3 glomerulopathy with complement blockers.
Emma et al., Roma, Italy. In Semin Thromb Hemost, 2014
C3 glomerulopathy (C3G) is a newly defined clinical entity comprising glomerular lesions with predominant C3 staining.
[Bacteriological profile and antibiotic treatment of postoperative peritonitis].
Houissa et al., In Arch Inst Pasteur Tunis, 2013
Thus, the ampicillin resistance was 87.14%, that the C3G was 33.80%, the Piperacillin to Tazobactam combination, was 36.5% and that the association Ticarcillin-clavulanic acid was 43.6%.
Mulberry ( sang shèn zǐ) and its bioactive compounds, the chemoprevention effects and molecular mechanisms in vitro and in vivo.
Wang et al., T'ai-chung-shih, Taiwan. In J Tradit Complement Med, 2013
Of the various compounds in ME, cyanidin 3-glucoside (C3G) is the most abundant, and the active compound studied in mulberry research.
The non-receptor tyrosine kinase Lyn controls neutrophil adhesion by recruiting the CrkL-C3G complex and activating Rap1 at the leading edge.
Wang et al., Urbana, United States. In J Cell Sci, 2011
Lyn controls spatial activation of Rap1 by recruiting the CrkL-C3G protein complex to the leading edge
Frequent somatic demethylation of RAPGEF1/C3G intronic sequences in gastrointestinal and gynecological cancer.
Perucho et al., Los Angeles, United States. In Int J Oncol, 2011
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
Cytoskeletal remodeling by C3G to induce neurite-like extensions and inhibit motility in highly invasive breast carcinoma cells.
Radha et al., Hyderābād, India. In Biochim Biophys Acta, 2011
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.
Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population.
Wang et al., Nanjing, China. In Diabetes Res Clin Pract, 2011
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.
TC-PTP dephosphorylates the guanine nucleotide exchange factor C3G (RapGEF1) and negatively regulates differentiation of human neuroblastoma cells.
Radha et al., Hyderābād, India. In Plos One, 2010
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.
Inhibitory receptor signaling via tyrosine phosphorylation of the adaptor Crk.
Long et al., Rockville, United States. In Immunity, 2008
Here, we showed that binding of inhibitory natural killer (NK) cell receptors to human leukocyte antigen (HLA) class I on target cells induced tyrosine phosphorylation of the adaptor Crk, concomitant with dephosphorylation of the guanine exchange factor Vav1. Furthermore, Crk dissociated from the guanine exchange factor C3G and bound to the tyrosine kinase c-Abl during inhibition.
Insulin-stimulated GLUT4 translocation requires the CAP-dependent activation of TC10.
Saltiel et al., Ann Arbor, United States. In Nature, 2001
Here we show that phosphorylated Cbl recruits the CrkII-C3G complex to lipid rafts, where C3G specifically activates the small GTP-binding protein TC10.
Rap1 mediates sustained MAP kinase activation induced by nerve growth factor.
Stork et al., Portland, United States. In Nature, 1998
Rap1 is activated by CRK adaptor proteins and the guanine-nucleotide-exchange factor C3G, and forms a stable complex with B-Raf, an activator of MAP kinase.
Maintenance of human T cell anergy: blocking of IL-2 gene transcription by activated Rap1.
Nadler et al., Boston, United States. In Science, 1997
The adapter protein CrkL was associated with both phosphorylated Cbl and the guanidine nucleotide-releasing factor C3G, which catalyzes guanosine triphosphate (GTP) exchange on Rap1.
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