Affinage

RAPGEF1

Rap guanine nucleotide exchange factor 1 · UniProt Q13905

Length
1077 aa
Mass
120.5 kDa
Annotated
2026-06-10
100 papers in source corpus 53 papers cited in narrative 52 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RAPGEF1 (C3G) is a guanine nucleotide exchange factor that couples adaptor-based signaling to Rap-family GTPase activation, governing cell adhesion, migration, and developmental morphogenesis (PMID:8524240, PMID:11432821). It is a specific GEF for Rap1, markedly stimulating GDP-to-GTP exchange in vitro and elevating Rap1-GTP in cells, with weaker activity toward related Ras-family GTPases including R-Ras and Rap2 (PMID:8524240, PMID:11432821); its activation of R-Ras specifically routes signaling to JNK via MLK family kinases (PMID:9430657, PMID:10777559). C3G is recruited and activated through proline-rich motifs in its central region that bind the N-terminal SH3 domains of the Crk/CrkL adaptors, which deliver C3G to membranes downstream of integrins, receptor tyrosine kinases, and immune receptors (PMID:7512734, PMID:7806500, PMID:9268367). Its catalytic Cdc25H domain is held in cis-autoinhibition by an intramolecular autoinhibitory region (AIR), and full GEF output requires a two-input mechanism: tyrosine phosphorylation at Y504 by Src-family kinases, Hck, or c-Abl relieves negative regulation, while direct Crk binding to segregated proline-rich sites both targets C3G to the plasma membrane and stimulates exchange activity; lymphoma AIR mutations that break autoinhibition cause constitutive Rap1 and LFA-1 activation (PMID:10318861, PMID:14551197, PMID:32873726, PMID:36737758). Upstream activating inputs include integrin adhesion, ALK and EGF/insulin signaling, Reelin-Dab1 in cortical neurons, Cbl-CrkL in immune cells, and TCR/CTLA-4 signaling (PMID:9840945, PMID:10657627, PMID:15062102, PMID:18809728, PMID:20190816, PMID:24396067). Through Rap1, C3G drives integrin-dependent adhesion and migration, cortical neuron multipolar-to-bipolar transition and migration, platelet activation and megakaryocyte differentiation, and is essential for early mouse embryogenesis and vascular maturation (PMID:11432821, PMID:12466202, PMID:18506028, PMID:22659131, PMID:27111087, PMID:30567575). C3G additionally exerts GEF-independent functions, including suppression of oncogene-induced ERK activation via PP2A recruitment and destabilization of β-catenin to limit TCF transcription (PMID:15077165, PMID:17825818, PMID:23486661).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1994 High

    Established C3G's molecular identity by showing it binds Crk/Grb2 SH3 domains through a proline-rich region and carries a Ras-GNRP-homologous C-terminus, defining it as an adaptor-coupled exchange-factor candidate.

    Evidence Bacterial fusion pull-down, mutational mapping, and yeast CDC25 complementation

    PMID:7512734 PMID:7806500

    Open questions at the time
    • GEF substrate not yet defined
    • specificity of Crk SH3 binding over other adaptors not fully resolved in cells
  2. 1995 High

    Defined the catalytic substrate, showing C3G is a specific GEF for Rap1 in vitro and in cells with only marginal activity on Ras and Ral.

    Evidence In vitro GDP-dissociation/GTP-γS binding assays and in vivo GTP-loading in COS7 cells

    PMID:8524240

    Open questions at the time
    • mechanism linking adaptor binding to catalysis unknown
    • physiological upstream activators not identified
  3. 1997 High

    Resolved how adaptors activate C3G, demonstrating Crk/CrkL/Grb2 act mainly by membrane recruitment rather than allosteric stimulation in vivo.

    Evidence In vivo Rap1 GTP-loading versus in vitro GEF assays with membrane-targeting and dominant-negative constructs in COS1 cells

    PMID:9268367

    Open questions at the time
    • did not reconcile later evidence for direct Crk stimulation of catalysis
    • phospho-regulation of activity not addressed
  4. 1999 High

    Identified the activating phospho-switch, showing Y504 phosphorylation relieves an internal negative regulatory domain to activate GEF output.

    Evidence Systematic tyrosine mutagenesis (aa 391-579) with CrkI co-expression and Rap1-GTP loading

    PMID:10318861

    Open questions at the time
    • structural basis of the negative regulatory domain not defined
    • kinase responsible in physiological settings not pinned down
  5. 2001 High

    Established the in vivo requirement for C3G, showing it is essential for cell adhesion and early embryogenesis and that its role is interchangeable with other Rap1-activating GEFs.

    Evidence Knockout/conditional mouse, adhesion/migration assays, rescue by active Rap1, Rap2, R-Ras and other GEFs

    PMID:11432821

    Open questions at the time
    • tissue-specific downstream effectors not dissected
    • GEF-independent contributions to phenotype not separated
  6. 2003 High

    Connected C3G to specific adhesion structures and vascular development, showing it is needed for integrin-β1/paxillin focal adhesion formation in vivo.

    Evidence Hypomorphic knock-in mouse, focal adhesion immunofluorescence, PDGF response assays

    PMID:12466202

    Open questions at the time
    • selectivity for β1- over β3-adhesions mechanistically unexplained
  7. 2004 Medium

    Defined GEF-independent functions, showing C3G's N-terminal Crk-binding domain suppresses ERK via PP2A recruitment, expanding its role beyond Rap1 activation.

    Evidence Focus/soft-agar assays, co-IP with PP2A and PP2A activity assays, okadaic acid

    PMID:15077165 PMID:17825818

    Open questions at the time
    • direct PP2A binding interface not mapped
    • single lab; reciprocal validation limited
  8. 2004 High

    Placed C3G in the Reelin-Dab1 neuronal pathway, showing Reelin activates a Dab1→Crk→C3G→Rap1 cascade in cortical neurons.

    Evidence Phospho-Dab1 affinity pull-down, co-IP, Rap1-GTP assay in primary cortical neurons

    PMID:15062102

    Open questions at the time
    • downstream Rap1 effectors in migration not identified at this stage
  9. 2008 High

    Demonstrated the developmental neuronal requirement, showing C3G is needed for preplate splitting, the multipolar-to-bipolar transition, and cortical neuron migration via Reelin-driven Rap1 activation.

    Evidence Conditional KO mice, Rap1-GTP after reelin, in utero imaging

    PMID:18506028 PMID:27111087

    Open questions at the time
    • effector linking Rap1 to cytoskeletal remodeling in migrating neurons not fully defined
  10. 2012 High

    Established a GEF-dependent role in hemostasis, showing C3G overexpression enhances and GEF-dead C3G impairs platelet activation downstream of PKC-Rap1.

    Evidence Platelet-specific transgenic mice (C3G and C3GΔCat), bleeding time, aggregation, Rap1 assays

    PMID:22659131

    Open questions at the time
    • upstream kinase coupling PKC to C3G not yet defined here
  11. 2012 Medium

    Extended GEF-independent regulation to Wnt signaling, showing C3G binds and destabilizes β-catenin to repress TCF transcription independent of GEF activity and GSK3β.

    Evidence Reciprocal co-IP, domain mapping, TCF reporter, proteasome inhibitor

    PMID:23486661

    Open questions at the time
    • mechanism of β-catenin destabilization unresolved
    • single-lab finding
  12. 2020 High

    Resolved the autoinhibition mechanism, showing an intramolecular AIR blocks the catalytic domain and CrkL activates by displacing it, with lymphoma AIR mutations causing constitutive activation.

    Evidence Intramolecular interaction mapping, nucleotide exchange assays, mutagenesis, Ba/F3 Rap1/LFA-1 readouts

    PMID:32873726

    Open questions at the time
    • high-resolution structure of the autoinhibited state not reported
    • interplay of AIR release with Y504 phosphorylation not fully quantified here
  13. 2020 High

    Defined platelet-specific phospho-regulation, showing PKC-Src drives Y504 phosphorylation, ERK supports it by inhibiting Shp2, and C3G feeds the P2Y12-PI3K-Rap1b and thrombin-TXA2 pathways.

    Evidence Platelet-specific KO mouse, pathway inhibitors, phospho-site assays

    PMID:32296045

    Open questions at the time
    • direct Shp2-C3G relationship not biochemically reconstituted
  14. 2023 High

    Integrated phosphorylation and adaptor inputs into a two-factor activation model, showing Crk binding to segregated proline sites both recruits and directly stimulates C3G while Y504 phosphorylation primes the enzyme.

    Evidence ITC, sedimentation velocity, GEF kinetics, pull-downs, and membrane translocation in Jurkat cells

    PMID:36737758

    Open questions at the time
    • full-length structural model of the activated complex not determined
    • in vivo verification across cell types incomplete

Open questions

Synthesis pass · forward-looking unresolved questions
  • How C3G's GEF-dependent Rap1 outputs are integrated with its GEF-independent nuclear, PP2A, and β-catenin functions to produce cell-type-specific outcomes remains unresolved.
  • no unified structural model of activated, membrane-bound C3G
  • spatial coordination of Golgi/cytoskeletal/nuclear pools not defined
  • physiological selection between Rap1 versus R-Ras outputs unclear

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Localization
GO:0005886 plasma membrane 3 GO:0005794 Golgi apparatus 2 GO:0005856 cytoskeleton 2 GO:0005634 nucleus 1
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-162582 Signal Transduction 4 R-HSA-1474244 Extracellular matrix organization 3 R-HSA-168256 Immune System 3 R-HSA-109582 Hemostasis 2
Partners
ABL1BCAR1CBLCRKCRKLHCKPPP2CARAP1A

Evidence

Reading pass · 52 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 C3G (RAPGEF1) was identified as a guanine nucleotide-releasing protein that binds to the SH3 domains of CRK and GRB2/ASH adaptor proteins via a proline-rich sequence in its center region. The C-terminal region of C3G shows homology to GNRPs for Ras and complemented loss of CDC25 function in yeast. Bacterial fusion protein pull-down, mutational analysis, yeast complementation assay Proceedings of the National Academy of Sciences of the United States of America High 7512734
1994 Four proline-rich sequences in the center region of C3G each individually bind to the N-terminal SH3 domain of c-Crk and v-Crk with high specificity and preferentially over other SH3 domains (including Grb2 SH3). Endogenous C3G co-precipitates with Crk from cell lysates. GST pull-down, in vitro binding assays, co-precipitation from cell lysates The Journal of biological chemistry High 7806500
1995 C3G is a specific guanine nucleotide exchange factor (GEF) for Rap1: it markedly stimulated GDP dissociation and GTP-γS binding to Rap1B in vitro, and induced accumulation of GTP-bound Rap1A in COS7 cells in vivo, while having only marginal effects on Ha-Ras, N-Ras, and RalA. In vitro GEF assay (GDP dissociation, GTP-γS binding), in vivo GTP-loading assay in COS7 cells Molecular and cellular biology High 8524240
1996 Following T cell receptor activation, Cbl becomes tyrosine phosphorylated and associates with CrkL via the Crk SH2 domain (inhibitable by pYDVP phosphopeptide); CrkL constitutively associates with C3G, and a fraction of C3G co-immunoprecipitates with Cbl in activated Jurkat T cells. Co-immunoprecipitation, phosphopeptide competition assay The Journal of biological chemistry Medium 8626543
1996 C3G selectively binds to the amino-terminal SH3 domain of Grb2 in vitro, but in primary B cells C3G associates constitutively with the CrkL adaptor rather than with Grb2, Shc, or CrkII, both before and after BCR stimulation. Yeast two-hybrid, GST fusion protein pull-down, co-immunoprecipitation from B cells The Journal of biological chemistry Medium 8621483
1997 Expression of Crk, CrkL, and Grb2 with C3G enhances C3G GEF activity toward Rap1 in vivo primarily by recruiting C3G to the cell membrane, not by allosteric activation; membrane targeting of Crk (farnesylation signal) compensated for the SH2 domain requirement, and Crk did not stimulate C3G GEF activity in vitro. In vivo Rap1 GTP-loading assay, in vitro GEF assay, dominant-negative and membrane-targeting constructs in COS1 cells The Journal of biological chemistry High 9268367
1997 v-Crk activates JNK via C3G: coexpression of C3G with v-Crk further enhanced JNK activity and transformation, while a dominant-negative C3G lacking the GEF domain abolished v-Crk-induced JNK activity and colony formation in NIH 3T3 cells. JNK kinase assay, dominant-negative C3G expression, colony formation assay Proceedings of the National Academy of Sciences of the United States of America Medium 9122199
1997 Insulin and EGF stimulation induces dissociation of the CrkII-C3G complex, correlating with a conformational change in Rap1; dissociation is driven by tyrosine phosphorylation of CrkII at Tyr221 (mutation Y221F prevents insulin-induced dissociation), and is reversed by PTP1B-mediated dephosphorylation. Co-immunoprecipitation, GST-C3G pull-down, mutagenesis, PTP1B dephosphorylation assay The Journal of biological chemistry Medium 9353263
1998 p130Cas SH3 domain directly binds C3G via a proline-rich site (APPKPPLP) N-terminal to the Crk-binding motifs; mutational analysis defined Pro1, Lys3, and Pro4 as critical for high-affinity interaction (consensus CasSH3-binding motif: XXPXKPX). Yeast two-hybrid, in vitro pull-down, in vivo co-immunoprecipitation, deletion/point mutagenesis The Journal of biological chemistry High 9748234
1998 Transformation suppressor activity of C3G maps to its N-terminal Crk-binding (SH3-b) domain and is independent of the catalytic CDC25-H domain; a C3G mutant lacking the catalytic domain (C3GΔCat) suppressed Ras/Raf/Sis oncogene-induced focus formation as effectively as full-length C3G. Focus formation assay, NIH3T3 transfection with deletion mutants Oncogene Medium 9482107
1998 C3G activates JNK1 through a Ras-independent pathway involving MLK family kinases (MLK3 and DLK): dominant-negative MLK3 and DLK blocked C3G-induced JNK1 activation, while dominant-negative Ras, Rac, or Pak did not. JNK1 kinase assay, dominant-negative constructs, co-expression in 293T cells The Journal of biological chemistry Medium 9430657
1998 Integrin-mediated cell adhesion to fibronectin induces tyrosine phosphorylation of C3G via CrkL in a cytoskeleton-dependent manner in normal 3T3 fibroblasts; this pathway is disrupted in Bcr/Abl-expressing cells, which show reduced CrkL-C3G complex formation. Co-immunoprecipitation, tyrosine phosphorylation assay, cytoskeletal disruption experiments Oncogene Medium 9840945
1999 C3G is activated by CrkI-mediated tyrosine phosphorylation at tyrosine 504: the C3G-Y504F mutant was markedly less phosphorylated and less activated by CrkI expression. Phosphorylation at Y504 relieves a cis-acting negative regulatory domain (aa 391–579) outside the catalytic region. Systematic mutagenesis of all 7 tyrosines in aa 391-579, CrkI co-expression, Rap1-GTP loading assay The Journal of biological chemistry High 10318861
1999 The CrkL-C3G complex mediates integrin-dependent hematopoietic cell adhesion to fibronectin via VLA-4 and VLA-5; the GEF activity of C3G is required (GEF-dead mutant abrogates CrkL-induced adhesion), and the N-terminal SH3 domain of CrkL (C3G-binding domain) is critical. Overexpression of C3G and deletion mutants, integrin-blocking antibodies, flow cytometry Blood Medium 10339478
1999 The CrkL-C3G complex links Cbl to downstream signaling after integrin ligation; overexpression of C3G (identified as the major CrkL SH3 N-terminal binding protein) enhances spontaneous migration of Ba/F3 hematopoietic cells. Co-immunoprecipitation, GFP-fusion migration assay, domain deletion analysis The Journal of biological chemistry Medium 10608804
1999 CrkL mediates Ras-dependent activation of the Raf/ERK pathway through C3G in hematopoietic cells stimulated with erythropoietin or IL-3; C3G GEF domain is required (GEF-dead mutant is inhibitory), and dominant-negative Ras blocks CrkL/C3G-induced ERK2 and Elk-1 activation. ERK1/2 kinase assay, Elk-1 reporter assay, Ras activation assay, dominant-negative constructs The Journal of biological chemistry Medium 10514505
2000 C3G activates JNK via R-Ras (not Rap1): constitutively active R-Ras activated JNK while Rap1(Val-12) did not; dominant-negative R-Ras blocked v-Crk-induced JNK activation and transformation; among Rap1-specific GEFs (CalDAG-GEFI, Epac), none activated JNK. JNK kinase assay, dominant-negative R-Ras, GEF specificity panel, NIH3T3 flat reversion assay The Journal of biological chemistry Medium 10777559
2000 Formation of the CrkII-C3G complex is regulated by integrins and inversely correlates with ERK activation: suspended cells (low ERK) contain a CrkII-C3G complex with elevated Rap1-GTP, while adherent cells (high ERK) dissociate the complex; CrkII Y109L mutation disrupts the complex and activates ERK; PTP1B C215S also disrupts the complex. Co-immunoprecipitation, Rap1-GTP pull-down, overexpression in CHO cells The Journal of biological chemistry Medium 10777617
2000 IFN-γ activates a signaling cascade in which c-Cbl is tyrosine phosphorylated, recruits CrkL via its SH2 domain, and CrkL then promotes activation of C3G (constitutively bound to CrkL via N-terminal SH3) leading to Rap1 activation. Co-immunoprecipitation, Rap1 activation assay, tyrosine phosphorylation assay Journal of immunology Medium 10657627
2001 C3G-dependent activation of Rap1 is required for cell adhesion and early mouse embryogenesis: C3G knockout mice die before E7.5; C3G-deficient fibroblasts show impaired cell adhesion, delayed spreading, and accelerated migration, which are rescued by active Rap1, Rap2, R-Ras, or other Rap1 GEFs (Epac, CalDAG-GEFI). Knockout mouse model, Cre-lox conditional deletion, Rap1 GTP-loading assay, cell adhesion and migration assays The EMBO journal High 11432821
2003 Hck tyrosine kinase directly interacts with C3G via its SH3 domain binding to the proline-rich region of C3G; co-expression of Hck and C3G induces caspase-1, -8, and -9-mediated apoptosis requiring Hck catalytic activity but not C3G GEF domain or Y504 phosphorylation. Hck phosphorylates C3G at Y504 in cells. Co-immunoprecipitation, SH3 domain-based interaction cloning, apoptosis assay, dominant-negative caspase constructs, phosphorylation assay with kinase-dead Hck The Journal of biological chemistry Medium 14551197
2003 C3G is required for vascular maturation and focal adhesion formation in mouse development: hypomorphic C3G embryos die ~E11.5 with vascular defects; C3G-deficient fibroblasts lack paxillin/integrin-β1-positive focal adhesions (but not integrin-β3-positive ones) and show abnormal PDGF-BB responses. Hypomorphic knock-in mouse model, immunofluorescence for focal adhesion markers, PDGF response assays Development High 12466202
2004 Tyrosine-phosphorylated C3G (pY504) localizes predominantly to the Golgi complex and subcortical actin cytoskeleton when phosphorylated by Hck or Src; cytoskeletal disruption by cytochalasin D abolishes peripheral pY504-C3G staining without affecting Golgi localization, suggesting spatially restricted activation. Immunofluorescence with phospho-specific antibody (pY504), cytochalasin D treatment, subcellular fractionation BMC cell biology Medium 15320955
2004 Reelin stimulation of cortical neurons activates a Dab1→CrkL/CrkI/CrkII→C3G→Rap1 signaling pathway: Reelin induces Crk family binding to phospho-Dab1 at Y220 and Y232, induces tyrosine phosphorylation of C3G, and activates Rap1. Phospho-affinity pull-down from embryonic brain extract, co-immunoprecipitation, Rap1-GTP assay, cortical neuron culture Current biology High 15062102
2004 In nectin-based cell-cell adhesion, Rap1 is activated via a c-Src-Crk-C3G signaling cascade at cell-cell contact sites; Rap1 activation (together with c-Src) is required for FRG-mediated Cdc42 activation and formation of adherens junctions. Inhibiting Crk, C3G, or Rap1 reduced AJ formation. Co-immunoprecipitation, dominant-negative constructs, Rap1 activation assay, immunofluorescence of AJ markers The Journal of biological chemistry Medium 15504743
2004 C3G suppresses oncogene-induced ERK activation and cyclin A expression via its N-terminal Crk-binding domain independent of GEF activity; C3G and C3GΔCat interact with PP2A phosphatases (confirmed by co-immunoprecipitation) and increase ERK-associated PP2A activity at the subcortical actin cytoskeleton. ERK phosphorylation assay, focus formation assay, soft agar assay, co-immunoprecipitation with PP2A, PP2A phosphatase activity assay, okadaic acid treatment Oncogene Medium 15077165 17825818
2006 C3G controls the size of the cerebral cortical neural precursor population by inhibiting the Ras/Akt pathway: C3G-deficient neuroepithelial cells show overproliferation, nuclear β-catenin accumulation, Akt/PKB activation, GSK3β inhibition, and fail to exit the cell cycle in response to growth factors. Conditional knockout mouse, Rap1 GTP-loading assay, Akt and GSK3β phosphorylation assays, β-catenin localization The EMBO journal High 16858399
2006 A novel truncated C3G isoform, p87C3G, is overexpressed in CML cells and co-immunoprecipitates with Bcr-Abl; the interaction involves the SH3-binding domain (first polyproline region) of p87C3G and the SH3 domain of Abl, and Bcr-Abl phosphorylates p87C3G in vitro. Co-immunoprecipitation, in vitro pull-down, in vitro kinase assay, domain mutagenesis Experimental cell research Medium 16443220
2007 C3G is required for c-Abl-induced filopodia formation during cell spreading on fibronectin; C3G promotes filopodia in a manner requiring Abl catalytic activity and N-WASP function but independent of Rho/Rac/Cdc42 dominant-negative inhibition. Cellular C3G interacts with c-Abl and enhances c-Abl cytoplasmic localization. RNAi knockdown, overexpression, dominant-negative GTPases, wiskostatin pharmacological inhibition, co-immunoprecipitation, immunofluorescence Experimental cell research Medium 17475248
2008 C3G is essential for cortical neuron migration and preplate splitting during brain development; C3G is activated by reelin in cortical neurons leading to Rap1 activation; C3G-deficient neurons arrest in a multipolar state and fail to migrate, with disrupted basement membrane and radial glial processes. Conditional KO mouse, Rap1 GTP-loading assay after reelin stimulation, in utero live imaging, immunofluorescence Development High 18506028
2008 WAVE2 complex regulates TCR-stimulated Rap1 activation via recruitment and activation of the CrkL-C3G exchange complex; Abl tyrosine kinase (associated with WAVE2) phosphorylates C3G on tyrosine, which is required for C3G GEF activity toward Rap1, leading to integrin clustering and affinity maturation. Co-immunoprecipitation, membrane recruitment assay, Rap1 activation assay, Abl kinase inhibitor, siRNA knockdown The Journal of cell biology Medium 18809728
2008 C3G promotes neurite growth in human neuroblastoma cells dependent on both its catalytic domain and N-terminal regulatory domain, requiring Cdc42 and Rap1 function; C3G knockdown inhibits forskolin- and NGF-induced differentiation; C3G is phosphorylated at Y504 predominantly in the Golgi upon forskolin/NGF treatment; C3G expression induces the cell cycle inhibitor p21. Overexpression and shRNA knockdown, dominant-negative GTPases, phospho-Y504 immunofluorescence, differentiation assays in IMR-32 cells Journal of neurochemistry Medium 18957052
2010 c-Abl phosphorylates C3G at Y504 in response to oxidative stress; this phosphorylation is dependent on the F-actin-binding domain (FABD) of c-Abl and is restricted to F-actin-rich regions; C3G knockdown or dominant-negative C3G inhibits c-Abl-mediated apoptosis. In vivo phosphorylation assay, FABD deletion mutant, RNAi, dominant-negative C3G, cytoskeletal fractionation Oncogene Medium 20581864
2010 Drosophila C3G is a Rap1-specific GEF (stimulates nucleotide exchange on Drosophila Rap GTPases in vitro) required for body wall muscle integrity and proper βPS integrin localization at muscle attachment sites during larval stages. In vitro GEF assay with Drosophila Rap GTPases, genetic deletion of C3G locus, in situ hybridization, immunofluorescence PloS one High 20209136
2010 ALK receptor tyrosine kinase activates Rap1 via C3G: activated ALK recruits a constitutive CrkL-C3G complex; siRNA knockdown of C3G or Rap1 inhibits ALK-induced neurite outgrowth and neuroblastoma cell proliferation. Co-immunoprecipitation, Rap1 activation assay, siRNA knockdown, Rap1GAP overexpression Oncogene Medium 20190816
2011 Lyn tyrosine kinase controls spatial activation of Rap1 at the neutrophil leading edge by recruiting the CrkL-C3G complex; depletion of Lyn prevents chemoattractant-induced Rap1 activation at the leading edge, rescued by ectopic Rap1 expression. RNAi depletion of Lyn, Rap1 activation assay, live imaging of leading edge localization, epistasis with Rap1 rescue Journal of cell science Medium 21628423
2011 TC-PTP (TC48 isoform) dephosphorylates C3G at Y504: TC48 interacts with C3G via its C-terminal non-catalytic residues and the Crk-binding region of C3G; a substrate-trap mutant of TC48 preferentially binds phospho-C3G at the Golgi; TC48 expression abrogates Src- and pervanadate-induced C3G phosphorylation and inhibits neurite outgrowth. Co-immunoprecipitation, substrate-trap mutant, in vitro dephosphorylation, IGF-induced dephosphorylation, neurite outgrowth assay PloS one Medium 21876762
2012 C3G plays a role in platelet clotting through its GEF activity: transgenic mice overexpressing C3G in platelets showed shorter bleeding times and stronger platelet activation, while tgC3GΔCat (GEF-dead) mice showed a bleeding diathesis; C3G is a mediator in the PKC pathway leading to Rap1 activation in platelets. Transgenic mouse model (platelet-specific), bleeding time assay, platelet aggregation assay, Rap1 activation assay Biochimica et biophysica acta High 22659131
2012 C3G forms a complex with Bcr-Abl and p38α MAPK at focal adhesions in CML cells; interactions involve SH3/SH3-b domains with CrkL, p130Cas, Cbl, and Abi1; C3G, Abi1, or Cbl knockdown impairs adhesion to fibronectin; C3G and p38α act through a common pathway to regulate K562 cell adhesion. Co-immunoprecipitation, immunofluorescence, siRNA knockdown, cell adhesion assay Cell communication and signaling Medium 23343344
2012 C3G functions as a negative regulator of β-catenin: C3G is present in a complex with β-catenin (via its proline-rich Crk-binding region interacting with β-catenin residues 90-525); C3G overexpression destabilizes β-catenin and reduces its nuclear accumulation and TCF transcription activity independent of GEF activity and GSK3β; β-catenin reciprocally represses C3G expression. Co-immunoprecipitation, deletion mutant mapping, TCF reporter assay, Western blot for β-catenin stability, proteasome inhibitor treatment Genes & cancer Medium 23486661
2014 CTLA-4 receptor signaling mediates tyrosine phosphorylation of C3G (facilitated by Hck), which is required for augmented Rap1 activation and LFA-1-mediated T-cell adhesion; C3G translocates to the plasma membrane downstream of TCR signaling in a Zap70-dependent manner. Co-immunoprecipitation, Rap1 activation assay, C3G membrane translocation assay, siRNA knockdown, Zap70 inhibitor Molecular and cellular biology Medium 24396067
2014 Immunophilin cyclophilin A increases C3G binding to CrkII, while immunophilin inhibitors (CsA, FK506) inhibit CrkII-C3G association by promoting cis-conformation of CrkII (detected by FRET); suppression of CrkII-C3G complex by immunophilin inhibitors impairs T cell adhesion to fibronectin and migration toward SDF-1α. Co-immunoprecipitation, FRET-based PICCHU assay, T cell adhesion and migration assay Journal of immunology Medium 25225668
2015 C3G-mediated Rap1 activation promotes secretion of MMP-2 and MMP-9 in ovarian cancer cells; C3G knockdown suppresses Rap1 activity and reduces MMP-2 and MMP-9 secretion as well as cell invasion. siRNA knockdown, Rap1 activation assay, MMP secretion assay, invasion assay Cancer letters Medium 25617801
2015 C3G promotes survival and myogenic differentiation of C2C12 cells through mechanisms requiring both its catalytic and protein interaction domains, dependent on cellular R-Ras; C3G localizes to focal adhesions in myotubes; C3G expression increases Akt activity and suppresses cyclin D1 while inducing p27. C2C12 differentiation assay, shRNA knockdown, dominant-negative C3G, R-Ras dependence assay, immunofluorescence Biochimica et biophysica acta Medium 26133694
2016 C3G is required in multipolar neurons for the multi-to-bipolar transition during cortical development: conditional inactivation of Rapgef1 results in defects in neuronal migration, axon formation, and cortical lamination; C3G is required for specification of an axon and initiation of radial migration. Conditional KO (Cre-mediated at different time points), in utero electroporation, live cell imaging PloS one High 27111087
2017 C3G regulates platelet α-granule exocytosis with both GEF-dependent and independent mechanisms; transgenic C3G platelets showed decreased secretion of anti-angiogenic factors; C3G interacts with VAMP-7 (vesicle-associated membrane protein), potentially explaining α-granule retention. Proteomic analysis of platelet secretome, in vitro capillary tube formation assay, in vivo tumor models, immunofluorescence, co-immunoprecipitation with VAMP-7 Oncotarget Medium 29340032
2017 C3G undergoes regulated nucleocytoplasmic exchange: it contains functional NLS, NES, and requires GSK3-β-dependent phosphorylation for nuclear localization; nuclear C3G associates with chromatin and nuclear matrix, represses euchromatin-associated histone modifications, and is required for myogenic differentiation. Leptomycin B treatment, importin-α co-expression, GSK3β inhibition, CRISPR/Cas9 KO, chromatin fractionation, ChIP-like histone modification assay Molecular biology of the cell Medium 28148649
2018 C3G, through its GEF activity, induces megakaryocytic differentiation and proplatelet formation: transgenic C3G (but not C3GΔCat) bone marrow cells showed increased megakaryocyte differentiation markers; GATA-1 was identified as a positive regulator of C3G expression. Transgenic mouse models (platelet-specific C3G and C3GΔCat), flow cytometry for differentiation markers, bone marrow explant proplatelet assay Cell communication and signaling Medium 30567575
2020 C3G autoinhibition is mediated by two intramolecular interactions: (1) an autoinhibitory region (AIR) in the central domain binds to and blocks the catalytic Cdc25H domain; (2) the N-terminal domain binding to the REM domain is required for GEF activity. CrkL activates C3G by displacing the AIR/Cdc25HD interaction. Two lymphoma missense mutations in the AIR (Y554H, M555K) disrupt autoinhibition and cause constitutive Rap1 and LFA-1 activation. Biochemical mapping of intramolecular interactions, nucleotide exchange assay, mutagenesis, Ba/F3 cell functional assay for Rap1 and LFA-1 activation Science signaling High 32873726
2020 C3G is phosphorylated at Y504 in platelets by a PKC-Src-dependent mechanism; ERKs positively regulate this phosphorylation by inhibiting the tyrosine phosphatase Shp2; C3G participates in the ADP-P2Y12-PI3K-Rap1b and thrombin-TXA2 pathways and inhibits TXA2 synthesis through cPLA2 regulation. Platelet-specific C3G KO mouse, Rap1 activation assay, specific pathway inhibitors, phosphorylation assays Signal transduction and targeted therapy High 32296045
2021 C3G is essential for embryonic stem cell differentiation and lineage commitment: C3G-null ES cells show elevated STAT3 activity, very low ERK activity, high self-renewal factor expression (KLF4, ESRRB), and fail to differentiate upon LIF withdrawal; reintroduction of C3G partially reverts these changes. C3G KO cells also show reduced pFAK, pPaxillin, and integrin-β1, and downregulation of adhesion genes. CRISPR/Cas9 KO, STAT3 and ERK activity assay, gene expression analysis, C3G rescue, teratoma assay Stem cell reviews and reports Medium 33624208
2023 Crk proteins activate C3G GEF activity via two segregated mechanisms: (1) recruitment to the plasma membrane via CrkL-SH3N binding to P1/P2 sites; (2) direct GEF stimulation via Crk binding to P3 (essential, occluded in resting C3G) and P4 sites. Tyrosine phosphorylation of C3G alone causes marginal activation but primes C3G by lowering the Crk concentration required for full activation and increasing maximum activity. CrkL-SH2 domain interaction with phospho-C3G is additionally required for optimal activation. Isothermal titration calorimetry, sedimentation velocity, nucleotide-dissociation kinetic assay, affinity pull-down, plasma membrane translocation assay in Jurkat cells Cell communication and signaling High 36737758

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1994 C3G, a guanine nucleotide-releasing protein expressed ubiquitously, binds to the Src homology 3 domains of CRK and GRB2/ASH proteins. Proceedings of the National Academy of Sciences of the United States of America 371 7512734
1995 Identification of Rap1 as a target for the Crk SH3 domain-binding guanine nucleotide-releasing factor C3G. Molecular and cellular biology 330 8524240
2001 c(3)G encodes a Drosophila synaptonemal complex protein. Genes & development 261 11731477
1982 Breakdown of C3 after complement activation. Identification of a new fragment C3g, using monoclonal antibodies. The Journal of experimental medicine 200 6177820
2001 Requirement for C3G-dependent Rap1 activation for cell adhesion and embryogenesis. The EMBO journal 180 11432821
1996 Stimulation through the T cell receptor induces Cbl association with Crk proteins and the guanine nucleotide exchange protein C3G. The Journal of biological chemistry 178 8626543
1994 Four proline-rich sequences of the guanine-nucleotide exchange factor C3G bind with unique specificity to the first Src homology 3 domain of Crk. The Journal of biological chemistry 175 7806500
2004 Activation of a Dab1/CrkL/C3G/Rap1 pathway in Reelin-stimulated neurons. Current biology : CB 165 15062102
1997 Downstream of Crk adaptor signaling pathway: activation of Jun kinase by v-Crk through the guanine nucleotide exchange protein C3G. Proceedings of the National Academy of Sciences of the United States of America 128 9122199
2004 Involvement of the c-Src-Crk-C3G-Rap1 signaling in the nectin-induced activation of Cdc42 and formation of adherens junctions. The Journal of biological chemistry 127 15504743
1996 Sos, Vav, and C3G participate in B cell receptor-induced signaling pathways and differentially associate with Shc-Grb2, Crk, and Crk-L adaptors. The Journal of biological chemistry 111 8621483
2019 Neuroprotective effects of anthocyanins and its major component cyanidin-3-O-glucoside (C3G) in the central nervous system: An outlined review. European journal of pharmacology 107 31238064
1999 The adapter protein Crkl links Cbl to C3G after integrin ligation and enhances cell migration. The Journal of biological chemistry 95 10608804
1999 Activation of C3G guanine nucleotide exchange factor for Rap1 by phosphorylation of tyrosine 504. The Journal of biological chemistry 94 10318861
1984 Physiologic inactivation of fluid phase C3b: isolation and structural analysis of C3c, C3d,g (alpha 2D), and C3g. Journal of immunology (Baltimore, Md. : 1950) 94 6607952
1997 Enhancement of guanine-nucleotide exchange activity of C3G for Rap1 by the expression of Crk, CrkL, and Grb2. The Journal of biological chemistry 91 9268367
2005 Juxtaposition of C(2)M and the transverse filament protein C(3)G within the central region of Drosophila synaptonemal complex. Proceedings of the National Academy of Sciences of the United States of America 88 15767569
2008 The WAVE2 complex regulates T cell receptor signaling to integrins via Abl- and CrkL-C3G-mediated activation of Rap1. The Journal of cell biology 84 18809728
1998 Insulin regulates the dynamic balance between Ras and Rap1 signaling by coordinating the assembly states of the Grb2-SOS and CrkII-C3G complexes. The EMBO journal 82 9564038
1999 CrkL activates integrin-mediated hematopoietic cell adhesion through the guanine nucleotide exchange factor C3G. Blood 81 10339478
1998 Direct binding of p130(Cas) to the guanine nucleotide exchange factor C3G. The Journal of biological chemistry 79 9748234
2008 C3G regulates cortical neuron migration, preplate splitting and radial glial cell attachment. Development (Cambridge, England) 70 18506028
1998 Development of highly selective SH3 binding peptides for Crk and CRKL which disrupt Crk-complexes with DOCK180, SoS and C3G. Oncogene 68 9591773
1998 Guanine-nucleotide exchange protein C3G activates JNK1 by a ras-independent mechanism. JNK1 activation inhibited by kinase negative forms of MLK3 and DLK mixed lineage kinases. The Journal of biological chemistry 65 9430657
2022 Alternative Complement Pathway Inhibition With Iptacopan for the Treatment of C3 Glomerulopathy-Study Design of the APPEAR-C3G Trial. Kidney international reports 64 36217526
2003 The guanine nucleotide exchange factor C3G is necessary for the formation of focal adhesions and vascular maturation. Development (Cambridge, England) 62 12466202
2003 Negative regulation of T cell antigen receptor-mediated Crk-L-C3G signaling and cell adhesion by Cbl-b. The Journal of biological chemistry 60 12697763
2000 IFN-gamma activates the C3G/Rap1 signaling pathway. Journal of immunology (Baltimore, Md. : 1950) 58 10657627
2000 Crk activation of JNK via C3G and R-Ras. The Journal of biological chemistry 58 10777559
1998 T cell receptor-mediated tyrosine phosphorylation of Cas-L, a 105-kDa Crk-associated substrate-related protein, and its association of Crk and C3G. The Journal of biological chemistry 57 9497377
2003 Physical and functional interaction between Hck tyrosine kinase and guanine nucleotide exchange factor C3G results in apoptosis, which is independent of C3G catalytic domain. The Journal of biological chemistry 56 14551197
2022 Clinical Outcomes of Patients with C3G or IC-MPGN Treated with the Factor D Inhibitor Danicopan: Final Results from Two Phase 2 Studies. American journal of nephrology 55 36423588
2020 Studies on the interactional characterization of preheated silkworm pupae protein (SPP) with anthocyanins (C3G) and their effect on anthocyanin stability. Food chemistry 53 32413765
1999 CrkL mediates Ras-dependent activation of the Raf/ERK pathway through the guanine nucleotide exchange factor C3G in hematopoietic cells stimulated with erythropoietin or interleukin-3. The Journal of biological chemistry 51 10514505
2018 Unraveling the Molecular Mechanisms Underlying Complement Dysregulation by Nephritic Factors in C3G and IC-MPGN. Frontiers in immunology 49 30487789
2011 Signalling to actin: role of C3G, a multitasking guanine-nucleotide-exchange factor. Bioscience reports 49 21366540
2015 The C3G/Rap1 pathway promotes secretion of MMP-2 and MMP-9 and is involved in serous ovarian cancer metastasis. Cancer letters 48 25617801
1999 Activation of the Drosophila C3G leads to cell fate changes and overproliferation during development, mediated by the RAS-MAPK pathway and RAP1. The EMBO journal 48 9878058
2002 Novel function of Chat in controlling cell adhesion via Cas-Crk-C3G-pathway-mediated Rap1 activation. Journal of cell science 47 12432078
2004 Phosphorylated guanine nucleotide exchange factor C3G, induced by pervanadate and Src family kinases localizes to the Golgi and subcortical actin cytoskeleton. BMC cell biology 41 15320955
1998 Transformation suppressor activity of C3G is independent of its CDC25-homology domain. Oncogene 41 9482107
2006 C3G regulates the size of the cerebral cortex neural precursor population. The EMBO journal 40 16858399
2007 C3G is required for c-Abl-induced filopodia and its overexpression promotes filopodia formation. Experimental cell research 37 17475248
2010 Anaplastic lymphoma kinase activates the small GTPase Rap1 via the Rap1-specific GEF C3G in both neuroblastoma and PC12 cells. Oncogene 36 20190816
2006 Characterization of p87C3G, a novel, truncated C3G isoform that is overexpressed in chronic myeloid leukemia and interacts with Bcr-Abl. Experimental cell research 35 16443220
2003 Src-CrkII-C3G-dependent activation of Rap1 switches growth hormone-stimulated p44/42 MAP kinase and JNK/SAPK activities. The Journal of biological chemistry 35 12734187
2004 C3G-mediated suppression of oncogene-induced focus formation in fibroblasts involves inhibition of ERK activation, cyclin A expression and alterations of anchorage-independent growth. Oncogene 34 15077165
2000 The association of CRKII with C3G can be regulated by integrins and defines a novel means to regulate the mitogen-activated protein kinases. The Journal of biological chemistry 34 10777617
2004 Amplification, up-regulation and over-expression of C3G (CRK SH3 domain-binding guanine nucleotide-releasing factor) in non-small cell lung cancers. Journal of human genetics 33 15138850
2007 The formation of the central element of the synaptonemal complex may occur by multiple mechanisms: the roles of the N- and C-terminal domains of the Drosophila C(3)G protein in mediating synapsis and recombination. Genetics 31 17947423
2016 Potential role of cyanidin 3-glucoside (C3G) in diabetic cardiomyopathy in diabetic rats: An in vivo approach. Saudi journal of biological sciences 29 29686513
2008 The guanine nucleotide exchange factor, C3G regulates differentiation and survival of human neuroblastoma cells. Journal of neurochemistry 29 18957052
2007 C3G mediated suppression of malignant transformation involves activation of PP2A phosphatases at the subcortical actin cytoskeleton. Experimental cell research 29 17825818
1998 C3G is tyrosine-phosphorylated after integrin-mediated cell adhesion in normal but not in Bcr/Abl expressing cells. Oncogene 29 9840945
2017 Optimization of Conditions for Cyanidin-3-OGlucoside (C3G) Nanoliposome Production by Response Surface Methodology and Cellular Uptake Studies in Caco-2 Cells. Molecules (Basel, Switzerland) 28 28335396
2024 C3G and Ig-MPGN-treatment standard. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 27 37604793
2021 Cyanidin-3-o-glucoside (C3G) inhibits vascular leakage regulated by microglial activation in early diabetic retinopathy and neovascularization in advanced diabetic retinopathy. Bioengineered 27 34699316
2017 C3G promotes a selective release of angiogenic factors from activated mouse platelets to regulate angiogenesis and tumor metastasis. Oncotarget 27 29340032
1997 Insulin and epidermal growth factor stimulate a conformational change in Rap1 and dissociation of the CrkII-C3G complex. The Journal of biological chemistry 27 9353263
2020 C3G contributes to platelet activation and aggregation by regulating major signaling pathways. Signal transduction and targeted therapy 26 32296045
2015 C3G (RapGEF1), a regulator of actin dynamics promotes survival and myogenic differentiation of mouse mesenchymal cells. Biochimica et biophysica acta 26 26133694
2010 C3G down-regulates p38 MAPK activity in response to stress by Rap-1 independent mechanisms: involvement in cell death. Cellular signalling 26 19925863
2006 Inactivation of Crk SH3 domain-binding guanine nucleotide-releasing factor (C3G) in cervical squamous cell carcinoma. International journal of gynecological cancer : official journal of the International Gynecological Cancer Society 26 16681758
2010 F-actin-binding domain of c-Abl regulates localized phosphorylation of C3G: role of C3G in c-Abl-mediated cell death. Oncogene 25 20581864
2016 C3G knock-down enhances migration and invasion by increasing Rap1-mediated p38α activation, while it impairs tumor growth through p38α-independent mechanisms. Oncotarget 24 27286263
2011 Frequent somatic demethylation of RAPGEF1/C3G intronic sequences in gastrointestinal and gynecological cancer. International journal of oncology 24 21399874
2018 How Rap and its GEFs control liver physiology and cancer development. C3G alterations in human hepatocarcinoma. Hepatic oncology 23 30302196
2016 C3G/Rapgef1 Is Required in Multipolar Neurons for the Transition to a Bipolar Morphology during Cortical Development. PloS one 23 27111087
2011 The non-receptor tyrosine kinase Lyn controls neutrophil adhesion by recruiting the CrkL-C3G complex and activating Rap1 at the leading edge. Journal of cell science 23 21628423
2009 C3G silencing enhances STI-571-induced apoptosis in CML cells through p38 MAPK activation, but it antagonizes STI-571 inhibitory effect on survival. Cellular signalling 23 19324082
2013 C3G forms complexes with Bcr-Abl and p38α MAPK at the focal adhesions in chronic myeloid leukemia cells: implication in the regulation of leukemic cell adhesion. Cell communication and signaling : CCS 22 23343344
2010 Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population. Diabetes research and clinical practice 22 21146886
2011 TC-PTP dephosphorylates the guanine nucleotide exchange factor C3G (RapGEF1) and negatively regulates differentiation of human neuroblastoma cells. PloS one 21 21876762
2018 C3G, through its GEF activity, induces megakaryocytic differentiation and proplatelet formation. Cell communication and signaling : CCS 18 30567575
2011 Cytoskeletal remodeling by C3G to induce neurite-like extensions and inhibit motility in highly invasive breast carcinoma cells. Biochimica et biophysica acta 18 21223981
2005 Interaction of Bcr/Abl with C3G, an exchange factor for the small GTPase Rap1, through the adapter protein Crkl. Biochemical and biophysical research communications 18 15982636
1998 Differential interaction of Crkl with Cbl or C3G, Hef-1, and gamma subunit immunoreceptor tyrosine-based activation motif in signaling of myeloid high affinity Fc receptor for IgG (Fc gamma RI). Journal of immunology (Baltimore, Md. : 1950) 18 9820532
1983 Further studies of the C3g component of the alpha 2D fragment of human C3. Clinical and experimental immunology 18 6602022
2022 Andrographolide suppresses osteoarthritis progression by regulating circ_Rapgef1/miR-383-3p/NLRP3 signaling axis. Transplant immunology 17 35122957
2021 Functional Characterization of Rare Genetic Variants in the N-Terminus of Complement Factor H in aHUS, C3G, and AMD. Frontiers in immunology 16 33519811
2014 Immunophilins control T lymphocyte adhesion and migration by regulating CrkII binding to C3G. Journal of immunology (Baltimore, Md. : 1950) 16 25225668
2012 C3G transgenic mouse models with specific expression in platelets reveal a new role for C3G in platelet clotting through its GEF activity. Biochimica et biophysica acta 16 22659131
2020 Mechanisms of autoregulation of C3G, activator of the GTPase Rap1, and its catalytic deregulation in lymphomas. Science signaling 15 32873726
2014 Cytotoxic-T-lymphocyte antigen 4 receptor signaling for lymphocyte adhesion is mediated by C3G and Rap1. Molecular and cellular biology 14 24396067
2013 Elevated expression of C3G protein in the peri-infarct myocardium of rats. Medical science monitor basic research 12 23291598
2010 The Rap1 guanine nucleotide exchange factor C3G is required for preservation of larval muscle integrity in Drosophila melanogaster. PloS one 12 20209136
2009 RAPGEF1 gene variants associated with type 2 diabetes in the Korean population. Diabetes research and clinical practice 12 19297053
2021 C3G Regulates STAT3, ERK, Adhesion Signaling, and Is Essential for Differentiation of Embryonic Stem Cells. Stem cell reviews and reports 11 33624208
2021 C3G downregulation induces the acquisition of a mesenchymal phenotype that enhances aggressiveness of glioblastoma cells. Cell death & disease 11 33824275
2023 Crk proteins activate the Rap1 guanine nucleotide exchange factor C3G by segregated adaptor-dependent and -independent mechanisms. Cell communication and signaling : CCS 10 36737758
2022 Formation, structure and stability of high internal phase Pickering emulsions stabilized by BSPI-C3G covalent complexes. Food chemistry: X 10 36203951
2020 The Effects of C3G and D3G Anthocyanin-Rich Black Soybean on Energy Metabolism in Beige-like Adipocytes. Journal of agricultural and food chemistry 10 33059446
2017 C3G shows regulated nucleocytoplasmic exchange and represses histone modifications associated with euchromatin. Molecular biology of the cell 10 28148649
2020 C3G Is Upregulated in Hepatocarcinoma, Contributing to Tumor Growth and Progression and to HGF/MET Pathway Activation. Cancers 9 32823931
2012 Reciprocal Negative Regulation between the Guanine Nucleotide Exchange Factor C3G and β-Catenin. Genes & cancer 9 23486661
2008 C3G overexpression in glomerular epithelial cells during anti-GBM-induced glomerulonephritis. Kidney international 9 18784646
2001 C3G, a guanine nucleotide exchange factor bound to adapter molecule c-Crk, has two alternative splicing forms. Biochemical and biophysical research communications 9 11485308
1999 Identification of a novel splice variant of C3G which shows tissue-specific expression. DNA and cell biology 9 10492401
2022 C3G down-regulation enhances pro-migratory and stemness properties of oval cells by promoting an epithelial-mesenchymal-like process. International journal of biological sciences 8 36263169
2020 Expression of a novel brain specific isoform of C3G is regulated during development. Scientific reports 8 33139841

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