Affinage

ARHGEF25

Rho guanine nucleotide exchange factor 25 · UniProt Q86VW2

Length
580 aa
Mass
63.8 kDa
Annotated
2026-06-09
34 papers in source corpus 26 papers cited in narrative 26 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

ARHGEF25 (p63RhoGEF/GEFT) is a Dbl-family guanine nucleotide exchange factor that couples Gαq/11-linked GPCR signaling to Rho-family GTPase activation, controlling actin cytoskeletal remodeling, smooth muscle contraction, and tissue differentiation (PMID:18096806, PMID:11861769, PMID:21885830). The full-length p63RhoGEF catalyzes GDP/GTP exchange selectively on RhoA in vitro, an activity that requires its PH domain and drives actin stress fiber formation and SRF-mediated transcription (PMID:11861769, PMID:15069594). Activation is governed by an autoinhibitory arrangement in which the PH domain restrains the catalytic DH domain; active Gαq/11 (but not Gα12/13) directly engages a conserved C-terminal extension of the PH domain, relieving this autoinhibition and activating RhoA, as defined by the Gαq–p63RhoGEF–RhoA ternary crystal structure and reconstituted biochemistry (PMID:18096806, PMID:17606614, PMID:15632174). N-terminal palmitoylation (Cys-23/25/26) targets the protein to the plasma membrane and is required for full basal activity, while a longer cytosolic isoform (p63RhoGEF619) requires both Gαq-driven membrane recruitment and allosteric activation for full activity (PMID:21832057, PMID:27833100). Endogenous p63RhoGEF is the dominant mediator of Gαq/11-coupled agonist (angiotensin II, endothelin-1, phenylephrine)-induced RhoA activation, Ca²⁺-sensitized contractile force, stress fiber formation, and cardiac fibroblast CTGF expression and tissue stiffening (PMID:21885830, PMID:20739613, PMID:26392029). The pathway is regulated by MLK3, which binds p63RhoGEF and limits Gαq-mediated RhoA activation independent of its kinase activity, and by RGS2, which accelerates Gαq–p63RhoGEF complex dissociation (PMID:18851832, PMID:24299002). The N-terminally truncated GEFT isoform additionally exchanges on Rac1 and Cdc42 in vitro and promotes neurite outgrowth, myogenesis, lens fiber differentiation, and—through Rac1/Cdc42–PAK1 signaling—epithelial–mesenchymal transition in rhabdomyosarcoma, indicating context-dependent substrate usage (PMID:12547822, PMID:15322108, PMID:21663592, PMID:31761617).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2002 High

    Established the core enzymatic identity: that p63RhoGEF is a RhoA-specific exchange factor requiring its PH domain, answering what GTPase it acts on and where it functions.

    Evidence In vitro nucleotide exchange assay, confocal localization, and stress fiber assay in fibroblasts/cardiac myoblasts

    PMID:11861769

    Open questions at the time
    • Did not identify the upstream activating signal
    • Mechanism of PH-domain requirement unresolved
  2. 2003 Medium

    Showed that the N-terminally truncated GEFT isoform has exchange activity for Rac1 and Cdc42, introducing the question of isoform-dependent substrate specificity.

    Evidence In vitro exchange assay, GST-PAK pull-down, and NIH3T3 focus/migration assays

    PMID:12547822

    Open questions at the time
    • Substrate specificity conflicts with RhoA-selective full-length data
    • Overexpression-based readouts
  3. 2004 High

    Resolved that p63RhoGEF and GEFT are isoforms of one gene and that both activate RhoA and SRF transcription in cells, unifying the gene identity.

    Evidence RT-PCR isoform detection, GTPase activation assays, SRF reporter, and C3 transferase inhibition

    PMID:15069594 PMID:15322108

    Open questions at the time
    • Context-dependence of Rac1/Cdc42 versus RhoA usage not fully reconciled
  4. 2005 High

    Identified the upstream activator: active Gαq/11, but not Gα12/13, directly binds p63RhoGEF and enhances RhoA activation, placing it in Gq-coupled GPCR signaling.

    Evidence Co-IP, Gq/11-coupled receptor stimulation, RhoA assays, and dominant-negative Gα mutants; plus C2C12/3T3L1 differentiation models for GEFT

    PMID:15632174 PMID:16314529

    Open questions at the time
    • Structural basis of Gαq binding not yet defined
    • Mechanism of autoinhibition relief unknown
  5. 2007 High

    Defined the activation mechanism at atomic resolution: Gαq engages the PH-domain C-terminal extension to relieve DH-domain autoinhibition, explaining how GPCR signals are transduced to RhoA.

    Evidence X-ray crystallography of the Gαq–p63RhoGEF–RhoA ternary complex and reconstituted biochemistry with purified proteins

    PMID:17606614 PMID:18096806

    Open questions at the time
    • Did not address membrane targeting requirements
    • Dynamics in living cells unresolved
  6. 2008 Medium

    Identified negative regulators: MLK3 scaffolds and limits Gαq-driven activation, and Bves dampens GEFT-mediated Rac1/Cdc42 signaling, revealing regulatory inputs beyond Gαq.

    Evidence Co-IP, kinase-dead MLK3 mutants, active GTPase pull-downs, and migration assays

    PMID:18541910 PMID:18851832

    Open questions at the time
    • Single-lab Co-IP for each interaction
    • Stoichiometry and competition with Gαq not quantified
  7. 2011 High

    Established that palmitoylation-driven plasma membrane localization is required for activity, and demonstrated the endogenous physiological role in vascular smooth muscle Ca²⁺ sensitization.

    Evidence Cys→Ser mutagenesis with palmitoylation/fractionation assays plus siRNA knockdown in portal vein with ex vivo force measurements

    PMID:20739613 PMID:21663592 PMID:21832057 PMID:21885830

    Open questions at the time
    • Palmitoyl acyltransferase responsible not identified
    • Tissue specificity of contractile coupling incomplete
  8. 2014 Medium

    Captured the activation dynamics in living cells and the role of RGS2, showing Gαq–p63RhoGEF complex kinetics track Gαq activity and RGS2 accelerates dissociation.

    Evidence FRET imaging in single living cells with GPCR stimulation and RGS2 co-expression; plus pathological pathway placement in osteoblast and breast cancer models

    PMID:23696743 PMID:23884432 PMID:24008316 PMID:24299002

    Open questions at the time
    • FRET interactions are single-lab
    • Quantitative contribution of RGS2 in vivo unknown
  9. 2016 Medium

    Distinguished isoform behavior, showing the cytosolic p63RhoGEF619 requires dual Gαq input (recruitment plus allosteric activation) whereas membrane-anchored p63RhoGEF580 is constitutively localized.

    Evidence Live-cell imaging, FRET, rapamycin-inducible recruitment, FRAP, and RhoA biosensors

    PMID:27833100

    Open questions at the time
    • Physiological role of distinct isoforms in tissues not established
  10. 2025 Low

    Extended the Gαq–ARHGEF25–RhoA axis to disease, linking a GNAQ mutation to loss of pathway activation and apoptosis in NK/T-cell lymphoma.

    Evidence Co-IP, RhoA pathway assays, and apoptosis readouts in lymphoma cells; plus EMT/autophagy roles in rhabdomyosarcoma

    PMID:31761617 PMID:34221974 PMID:41362935

    Open questions at the time
    • Single Co-IP without reciprocal validation
    • Mechanism of mutation-dependent loss not structurally resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the conflicting RhoA versus Rac1/Cdc42 substrate selectivity of full-length and truncated isoforms is determined in physiological contexts, and what endogenous loss-of-function reveals beyond the second heart field, remain unresolved.
  • No in vivo whole-organism phenotype beyond a dispensable second-heart-field knockout (22449701)
  • Structural basis of isoform-specific substrate switching unknown
  • Endogenous determinants of Rac1/Cdc42 versus RhoA usage uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 3
Localization
GO:0005829 cytosol 3 GO:0005886 plasma membrane 3 GO:0005856 cytoskeleton 2 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-397014 Muscle contraction 2
Partners
BVESGNA11GNAQGPR116MLK3RGS2RHOA
Complex memberships
Gαq–p63RhoGEF–RhoA ternary complex

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 Crystal structure of the Gαq–p63RhoGEF–RhoA ternary complex revealed that Gαq engages p63RhoGEF via its effector-binding site and C-terminal region, and that this interaction relieves autoinhibition of the catalytic DH domain imposed by the adjacent PH domain, thereby activating RhoA. X-ray crystallography of ternary complex; functional validation in vitro and in intact cells Science High 18096806
2007 Activated Gαq directly relieves autoinhibition of p63RhoGEF by interacting with a highly conserved C-terminal extension of the PH domain; basally, the DH domain is autoinhibited by the PH domain. Biochemical/biophysical assays with purified proteins; deletion and mutant analysis The Journal of biological chemistry High 17606614
2005 Active Gαq or Gα11, but not Gα12 or Gα13, directly interacts with p63RhoGEF at its C-terminal half and strongly enhances p63RhoGEF-induced RhoA activation; this activation is independent of and competes with canonical phospholipase Cβ activation. Co-immunoprecipitation; Gq/11-coupled receptor stimulation (M3-cholinoceptor, H1 receptor); RhoA activation assays; dominant-negative Gα mutants The Journal of biological chemistry High 15632174
2002 p63RhoGEF specifically catalyzes GDP/GTP exchange on RhoA (not Rac1 or Cdc42) in vitro; RhoA activation in intact cells requires the presence of the PH domain; p63RhoGEF is localized to the sarcomeric I-band (cardiac sarcomeric actin) in human heart. In vitro guanine nucleotide exchange assay; confocal immunocytochemistry; stress fiber formation assay in fibroblasts and cardiac myoblasts Journal of cell science High 11861769
2004 p63RhoGEF and GEFT are isoforms encoded by the same gene; when expressed in cells both activate RhoA (not Rac1 or Cdc42) and induce SRF-mediated gene transcription in a C3-transferase-sensitive (Rho-dependent) manner, and both induce actin stress fibers. RT-PCR for isoform detection; RhoA/Rac1/Cdc42 activation assays; SRF reporter assay; C3 transferase inhibition; actin stress fiber morphology Naunyn-Schmiedeberg's archives of pharmacology High 15069594
2003 GEFT (N-terminally truncated isoform of ARHGEF25) has exchange activity for Rac1 and Cdc42 in vitro and promotes foci formation, cell proliferation, migration, and actin cytoskeletal reorganization (filopodia, lamellipodia) upon overexpression in NIH3T3 cells. In vitro GTPase exchange assay; GST-PAK pull-down for GTP-bound Rac1/Cdc42; NIH3T3 focus formation; cell proliferation and migration assays The Journal of biological chemistry Medium 12547822
2004 GEFT promotes neurite outgrowth in neuroblastoma cells via activation of Rac1, Cdc42, and RhoA; neurite outgrowth is primarily mediated by Rac1 and requires downstream effectors PAK1 and PAK5; GEFT also promotes dendritic spine enlargement in hippocampal neurons. GTP-bound GTPase pull-down; dominant-negative constructs; PAK1/PAK5 expression; Neuro2A cell neurite outgrowth assay; hippocampal neuron morphology The Journal of biological chemistry Medium 15322108
2005 GEFT promotes myogenesis of C2C12 cells via activation of RhoA, Rac1, and Cdc42 and their downstream effectors; a dominant-negative GEFT mutant inhibits myogenesis; GEFT inhibits insulin-induced adipogenesis in 3T3L1 preadipocytes; endogenous GEFT protein levels are modulated during skeletal muscle regeneration in vivo. Gene transfer in cardiotoxin-injured mouse tibialis anterior; C2C12 differentiation assay; dominant-negative mutant; GTPase activation assays; 3T3L1 adipogenesis assay Molecular and cellular biology Medium 16314529
2008 Bves (an integral membrane protein) directly physically interacts with GEFT; Bves expression reduces Rac1 and Cdc42 (but not RhoA) activity, and alters cell locomotion speed and cell roundness, positioning Bves as a negative regulator of GEFT-mediated Rac1/Cdc42 signaling. Co-immunoprecipitation; colocalization in adult skeletal muscle; active Rac1/Cdc42/RhoA pull-down assays; cell morphology and migration assays Proceedings of the National Academy of Sciences Medium 18541910
2008 MLK3 (a MAP3K) binds directly to p63RhoGEF/GEFT and thereby prevents Gαq from activating p63RhoGEF, limiting RhoA activation; this scaffolding function of MLK3 is independent of its kinase activity and is required for normal cell migration. Co-immunoprecipitation; kinase-dead MLK3 mutants; RhoA activation assays; cell migration assays Molecular cell Medium 18851832
2011 p63RhoGEF is palmitoylated at N-terminal cysteines (Cys-23/25/26); this palmitoylation is required for plasma membrane localization and for full basal GEF activity in cells; mutation of these cysteines to serine relocates p63RhoGEF to the cytoplasm and reduces basal activity, which can be rescued by forced membrane targeting or co-expression with wild-type (but not palmitoylation-deficient) Gαq. Site-directed mutagenesis (Cys→Ser); subcellular fractionation; palmitoylation assay; RhoA activation assays; rapamycin-inducible membrane-recruitment rescue The Journal of biological chemistry High 21832057
2011 p63RhoGEF selectively couples Gαq/11 (but not Gα12/13) to RhoA activation in vascular smooth muscle; silencing endogenous p63RhoGEF in mouse portal vein preferentially reduces contractile force induced by the Gαq/11-coupled agonist endothelin-1 and phenylephrine over the Gα12/13-coupled agonist U46619; introduction of the isolated PH domain of p63RhoGEF into permeabilized rabbit portal vein inhibited Ca2+-sensitized force and RhoA activation. siRNA knockdown in mouse portal vein; ex vivo force measurements; permeabilized tissue PH-domain introduction; RhoA activation assays Circulation research High 21885830
2010 In rat aortic smooth muscle cells, endogenous p63RhoGEF is the dominant mediator of fast angiotensin II–induced (Gq/11-dependent) RhoA activation; its knockdown abolished ANG II-induced stress fiber formation and cell elongation, reduced the mitogenic response, and impaired ANG II-driven contraction in a 3-D collagen model; p63RhoGEF did not activate Rac1 in this context. siRNA knockdown; RhoA/Rac1 activation assays; 2-D cell morphology; 3-D collagen contraction model; proliferation assay FASEB journal High 20739613
2009 p63RhoGEF binds to constitutively active Gα16QL (a Gαq family member) via Co-IP; overexpressed p63RhoGEF competitively displaces PLCβ2 and TTC1 from Gα16QL, inhibiting IP3 production, Ras activation, STAT3 phosphorylation, and SRE transcriptional activation. Co-immunoprecipitation in HEK293 cells; IP3 production assay; STAT3 phosphorylation; SRE luciferase reporter; competition binding assays Cellular signalling Medium 19332116
2013 Pasteurella multocida toxin inhibits osteoblast differentiation via Gαq/11 activation of p63RhoGEF, which activates RhoA; activated RhoA then transactivates the MAP kinase cascade (Rho kinase → Ras → MEK → ERK), blocking osteoblast differentiation; p63RhoGEF does not interact with Gα12/13 or Gαi in this pathway. Primary osteoblast and ST-2 cell differentiation models; alkaline phosphatase assay; mineralization nodule formation; pharmacological inhibitors; siRNA; GTPase activation assays PLoS pathogens Medium 23696743
2013 GPR116 (adhesion GPCR) promotes breast cancer cell migration, invasion, and lamellipodia/stress fiber formation through the Gαq–p63RhoGEF–RhoA/Rac1 pathway; GPR116 knockdown reduces RhoA and Rac1 activation, and p63RhoGEF knockdown phenocopies GPR116 knockdown. siRNA knockdown of GPR116 and p63RhoGEF; RhoA/Rac1 activation assays; cell migration and invasion assays; mouse mammary tumor metastasis models Cancer research Medium 24008316
2014 FRET-based live-cell imaging showed that Gαq and p63RhoGEF form a direct, dynamic complex upon GPCR activation; on/off kinetics of the Gαq–p63RhoGEF interaction closely match Gαq activity kinetics; RGS2 accelerates both Gαq deactivation and Gαq–p63RhoGEF complex dissociation; activation-dependent FRET between RGS2 and p63RhoGEF was detected, supporting a functional Gαq–p63RhoGEF–RGS2 complex. FRET (Gαq-CFP/Venus-p63RhoGEF) in single living cells; GPCR stimulation (H1, M3); RGS2 co-expression; downstream signaling assays The Biochemical journal Medium 24299002
2016 Three ARHGEF25 isoforms exist (p63RhoGEF580, GEFT, p63RhoGEF619); p63RhoGEF580 is constitutively plasma-membrane-localized while p63RhoGEF619 is cytosolic and translocates to the plasma membrane upon Gαq-coupled GPCR stimulation; both activate RhoA similarly after GPCR stimulation; synthetic membrane recruitment of p63RhoGEF619 increases RhoGEF activity but full activation requires allosteric activation by Gαq, revealing a dual role for Gαq (recruitment + allosteric activation) for cytosolic isoforms. Live-cell imaging; FRET; rapamycin-inducible membrane recruitment; FRAP (diffusion coefficients); RhoA activity FRET biosensor; GPCR stimulation Scientific reports Medium 27833100
2013 p63RhoGEF (plasma membrane) signals more efficiently downstream of Gαq than GEFT (cytoplasmic); forced membrane recruitment of GEFT via rapamycin-inducible system restores efficient Gαq-mediated signaling; membrane localization increases effective concentration rather than encounter time. Live-cell imaging; FRET-based calcium signaling assay; rapamycin-dependent membrane recruitment; FRAP for diffusion coefficients Scientific reports Medium 23884432
2006 GEFT protein is concentrated at actin-enriched regions in retinoic acid-induced primary neurites and at the growth cone tip in cAMP-induced axon-like extensions; GEFT promotes neurite outgrowth in both undifferentiated and differentiated Neuro2A cells. Immunofluorescence/confocal localization in differentiating Neuro2A cells; neurite outgrowth quantification with RA and dbcAMP treatment Journal of neuroscience research Low 16496360
2011 GEFT promotes lens fiber differentiation (cell elongation, lentoid formation, crystallin expression) in N/N1003A lens epithelial cells via a Rac1-dependent mechanism; Rac1 nuclear localization is required; pharmacological inhibition of Rac1 blocks GEFT-induced differentiation in ex vivo mouse lens explants. Transfection of lens epithelial cells; crystallin promoter luciferase assays; Rac1 inhibitor (NSC23766); ex vivo lens explant; immunohistochemistry Current molecular medicine Medium 21663592
2015 In cardiac fibroblasts, p63RhoGEF mediates angiotensin II-dependent RhoA activation, serum response factor activation, and CTGF expression/secretion; p63RhoGEF is localized to the trans-Golgi network in cardiac fibroblasts; its expression in engineered heart/connective tissue models increases tissue stiffness and contractile tension. siRNA knockdown; dominant-negative p63ΔN; RhoA activation assays; SRF reporter; CTGF ELISA; engineered heart muscle and connective tissue models; confocal colocalization Journal of molecular and cellular cardiology Medium 26392029
2019 GEFT activates the Rac1/Cdc42-PAK1 signaling pathway to promote EMT (upregulation of N-cadherin, Snail, Slug, Twist, Zeb1, Zeb2; downregulation of E-cadherin) and thereby drives rhabdomyosarcoma invasion and metastasis; GEFT gene promoter hypomethylation is associated with elevated GEFT expression in RMS. RMS cell lines; BALB/c nude mouse xenografts; siRNA/overexpression; active Rac1/Cdc42 assays; EMT marker western blot; bisulfite sequencing for methylation EBioMedicine Medium 31761617
2021 GEFT inhibits autophagy and apoptosis in rhabdomyosarcoma cells via Rac1/Cdc42 activation of mTOR; Rac1/Cdc42 inhibition reduces the anti-autophagy/anti-apoptosis effect of GEFT. GEFT overexpression/knockdown in RMS cells; Rac1/Cdc42 inhibitor; autophagy markers (Beclin1, LC3); apoptosis markers (Bcl-2, Bax); mTOR activity assays Frontiers in oncology Low 34221974
2025 GNAQ forms a complex with ARHGEF25 (Co-IP) and promotes RhoA activation in NK/T-cell lymphoma; GNAQ T96S mutation abolishes wild-type GNAQ ability to activate the GNAQ-ARHGEF25-RhoA pathway and trigger apoptosis. Co-immunoprecipitation; mRNA sequencing; Western blotting; RhoA pathway activity; CCK-8 and flow cytometry Cancer biology & therapy Low 41362935
2012 Conditional knockout of Geft in the second heart field (using Mef2c-Cre) results in mice that develop normally with no discernible cardiac phenotype, indicating Geft is dispensable for second heart field development. Conditional knockout mouse (loxP-flanked exons 5-17, Mef2c-Cre); cardiac morphology assessment BMB reports Medium 22449701

Source papers

Stage 0 corpus · 34 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Structure of Galphaq-p63RhoGEF-RhoA complex reveals a pathway for the activation of RhoA by GPCRs. Science (New York, N.Y.) 181 18096806
2005 The guanine nucleotide exchange factor p63RhoGEF, a specific link between Gq/11-coupled receptor signaling and RhoA. The Journal of biological chemistry 164 15632174
2007 Galphaq directly activates p63RhoGEF and Trio via a conserved extension of the Dbl homology-associated pleckstrin homology domain. The Journal of biological chemistry 118 17606614
2013 GPR116, an adhesion G-protein-coupled receptor, promotes breast cancer metastasis via the Gαq-p63RhoGEF-Rho GTPase pathway. Cancer research 95 24008316
2003 A Rac/Cdc42-specific exchange factor, GEFT, induces cell proliferation, transformation, and migration. The Journal of biological chemistry 71 12547822
2004 GEFT, a Rho family guanine nucleotide exchange factor, regulates neurite outgrowth and dendritic spine formation. The Journal of biological chemistry 70 15322108
2005 Modulation of muscle regeneration, myogenesis, and adipogenesis by the Rho family guanine nucleotide exchange factor GEFT. Molecular and cellular biology 69 16314529
2011 p63RhoGEF couples Gα(q/11)-mediated signaling to Ca2+ sensitization of vascular smooth muscle contractility. Circulation research 60 21885830
2008 Bves directly interacts with GEFT, and controls cell shape and movement through regulation of Rac1/Cdc42 activity. Proceedings of the National Academy of Sciences of the United States of America 57 18541910
2014 Increased level of p63RhoGEF and RhoA/Rho kinase activity in hypertensive patients. Journal of hypertension 54 24356540
2010 p63RhoGEF--a key mediator of angiotensin II-dependent signaling and processes in vascular smooth muscle cells. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 52 20739613
2002 Human p63RhoGEF, a novel RhoA-specific guanine nucleotide exchange factor, is localized in cardiac sarcomere. Journal of cell science 52 11861769
2004 p63RhoGEF and GEFT are Rho-specific guanine nucleotide exchange factors encoded by the same gene. Naunyn-Schmiedeberg's archives of pharmacology 43 15069594
2008 MLK3 limits activated Galphaq signaling to Rho by binding to p63RhoGEF. Molecular cell 40 18851832
2012 p63RhoGEF: a new switch for G(q)-mediated activation of smooth muscle. Trends in cardiovascular medicine 33 22902181
2019 Epigenetically upregulated GEFT-derived invasion and metastasis of rhabdomyosarcoma via epithelial mesenchymal transition promoted by the Rac1/Cdc42-PAK signalling pathway. EBioMedicine 31 31761617
2013 Pasteurella multocida toxin prevents osteoblast differentiation by transactivation of the MAP-kinase cascade via the Gα(q/11)--p63RhoGEF--RhoA axis. PLoS pathogens 25 23696743
2006 The Rho-family guanine nucleotide exchange factor GEFT enhances retinoic acid- and cAMP-induced neurite outgrowth. Journal of neuroscience research 21 16496360
2016 Kinetics of recruitment and allosteric activation of ARHGEF25 isoforms by the heterotrimeric G-protein Gαq. Scientific reports 19 27833100
2011 Plasma membrane association of p63 Rho guanine nucleotide exchange factor (p63RhoGEF) is mediated by palmitoylation and is required for basal activity in cells. The Journal of biological chemistry 18 21832057
2020 MicroRNA-29 family inhibits rhabdomyosarcoma formation and progression by regulating GEFT function. American journal of translational research 15 32269740
2015 p63RhoGEF regulates auto- and paracrine signaling in cardiac fibroblasts. Journal of molecular and cellular cardiology 15 26392029
2009 The RhoA-specific guanine nucleotide exchange factor p63RhoGEF binds to activated Galpha(16) and inhibits the canonical phospholipase Cbeta pathway. Cellular signalling 13 19332116
2021 GEFT Inhibits Autophagy and Apoptosis in Rhabdomyosarcoma via Activation of the Rac1/Cdc42-mTOR Signaling Pathway. Frontiers in oncology 12 34221974
2019 MicroRNA-874 functions as a tumor suppressor in rhabdomyosarcoma by directly targeting GEFT. American journal of cancer research 12 31105995
2013 Signaling efficiency of Gαq through its effectors p63RhoGEF and GEFT depends on their subcellular location. Scientific reports 11 23884432
2011 GEFT, A Rho family guanine nucleotide exchange factor, regulates lens differentiation through a Rac1-mediated mechanism. Current molecular medicine 11 21663592
2014 Dynamics of Gαq-protein-p63RhoGEF interaction and its regulation by RGS2. The Biochemical journal 10 24299002
2024 Lnc-PSMA8-1 activated by GEFT promotes rhabdomyosarcoma progression via upregulation of mTOR expression by sponging miR-144-3p. BMC cancer 4 38225540
2017 Gαq/p63RhoGEF interaction in RhoA/Rho kinase signaling: investigation in Gitelman's syndrome and implications with hypertension. Journal of endocrinological investigation 4 28840514
2019 GEFT aberrant expression in soft tissue sarcomas. Translational cancer research 2 35116743
2024 GEFT inhibits the GSDM-mediated proptosis signalling pathway, promoting the progression and drug resistance of rhabdomyosarcoma. Cell death & disease 1 39616223
2012 Geft is dispensable for the development of the second heart field. BMB reports 1 22449701
2025 GNAQ inhibits tumorigenesis via the ARHGEF25-mediated RHOA pathway in NK/T-cell lymphoma. Cancer biology & therapy 0 41362935

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