Affinage

RAC3

Ras-related C3 botulinum toxin substrate 3 · UniProt P60763

Round 2 corrected
Length
192 aa
Mass
21.4 kDa
Annotated
2026-04-28
108 papers in source corpus 39 papers cited in narrative 39 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RAC3 is a Rho-family small GTPase that functions as a molecular switch in actin cytoskeleton remodeling, cell invasion, neuronal migration, and dendritic spine morphogenesis, with roles distinct from and sometimes opposing those of its paralogue Rac1. RAC3 cycles between GTP- and GDP-bound states regulated by GAPs (including Bcr) and GEFs (including Vav2 downstream of phospho-cortactin/CCR7 at invadopodia), and signals through PAK1, JNK, p38 MAPK, and NF-κB pathways; PAK1 is the critical effector for DNA synthesis in breast cancer cells and for cortical neuron migration during corticogenesis (PMID:10618392, PMID:35851598, PMID:28356423). RAC3 opposes integrin-mediated cell-matrix adhesion through a GIT1–Arf6 axis and negatively regulates autophagy in an isoform-specific manner (PMID:19494130, PMID:21852230). De novo gain-of-function missense variants in RAC3 GTPase switch regions cause a neurodevelopmental disorder with structural brain malformations (NEDBAF), with variant-specific biochemical profiles ranging from constitutive activation to signaling-deficient alleles, all disrupting cortical neuron migration in vivo (PMID:35851598, PMID:35595279, PMID:41090727).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1997 High

    Cloning of RAC3 as a third Rac family member established it as a functional GTPase regulated by Bcr-GAP activity that signals to JNK upon constitutive activation, distinguishing it from Rac1/Rac2 by its unique C-terminal domain and serum-inducible expression.

    Evidence Molecular cloning, GTPase activity assays, JNK reporter, and immunoblotting in mammalian cells

    PMID:9252344

    Open questions at the time
    • Endogenous activating stimuli upstream of Rac3 not identified
    • Physiological effector specificity versus Rac1 unknown
  2. 2000 High

    Detection of hyperactive endogenous Rac3 in breast cancer cells revealed that Rac3 drives proliferation through a PAK-dependent pathway separable from JNK, establishing PAK as the critical mitogenic effector.

    Evidence GTP-Rac3 pulldown assays, dominant-negative PAK1 and Rac3 constructs, DNA synthesis assays in breast cancer cell lines

    PMID:10618392

    Open questions at the time
    • Identity of the GEF activating Rac3 in breast cancer not determined
    • In vivo relevance of the PAK-proliferation axis not tested
  3. 2001 High

    Identification of CIB as a Rac3-specific interactor (not binding Rac1/Rac2) linked Rac3 to integrin αIIbβ3-mediated adhesion, revealing isoform-selective signaling in adhesion/spreading.

    Evidence Reciprocal Co-IP, GST pulldown, GTPase pulldown, adhesion/spreading assays

    PMID:11756406

    Open questions at the time
    • Downstream signaling from Rac3–CIB complex not characterized
    • In vivo adhesion phenotype not assessed
  4. 2003 High

    Multiple studies established Rac3's transforming capacity (focus formation, anchorage-independent growth requiring cyclin D1 via the N43D effector domain), its requirement for geranylgeranylation, its developmental expression peaking during neuronal synaptogenesis, and its in vivo role in mammary gland differentiation and involution through PAK1 and p38 MAPK.

    Evidence Prenylation mutants with transformation assays, effector domain mutants with reporter assays, Rac3-specific antibody neuroanatomy, MMTV-V12Rac3 transgenic mice

    PMID:14605486 PMID:14622142 PMID:14633727

    Open questions at the time
    • Effector domain mutant studies refined later (2005) but N43D–cyclin D1 link mechanistically incomplete
    • How Rac3 opposes involution/apoptosis via p38 not resolved
  5. 2005 High

    Rac3 knockout mice revealed a non-redundant CNS role (enhanced motor coordination) and a stimulatory role in BCR/ABL leukemia; concurrently, siRNA studies showed Rac3 selectively controls cell invasion without affecting lamellipodia, distinguishing it functionally from Rac1.

    Evidence Rac3 KO mice behavioral tests, Rac3 KO × BCR/ABL transgenic survival analysis, isoform-specific siRNA in glioblastoma and breast carcinoma with invasion/lamellipodia assays

    PMID:15964829 PMID:15964830 PMID:16027728

    Open questions at the time
    • Molecular basis of enhanced motor coordination in Rac3 KO unclear
    • Invasion-specific effectors of Rac3 not identified at this point
  6. 2006 High

    Identification of Neurabin I as a direct Rac3 partner at neurite growth cones, required for Rac3-induced neuritogenesis, provided the first mechanism linking Rac3 to actin-based neuronal morphogenesis.

    Evidence Yeast two-hybrid confirmed by co-fractionation, antisense knockdown with domain-mutant rescue in neuronal cells

    PMID:16525025

    Open questions at the time
    • Whether Neurabin I mediates Rac3 invasion functions in non-neuronal cells untested
    • Signaling downstream of Rac3–Neurabin I not dissected
  7. 2007 High

    Demonstration that Rac1 and Rac3 have opposing effects on cell-matrix adhesion, governed by C-terminal residues 185–187 that dictate their distinct subcellular localizations (plasma membrane vs. perinuclear), resolved how two nearly identical GTPases generate antagonistic outputs.

    Evidence Isoform-specific siRNA, C-terminal chimeric mutants, adhesion and morphology assays in N1E-115 neuronal cells

    PMID:17244648

    Open questions at the time
    • In vivo validation of the opposing adhesion model lacking
    • How perinuclear Rac3 sends adhesion-disruptive signals not fully resolved
  8. 2009 High

    Discovery that Rac3 engages GIT1 independently of βPix (unlike Rac1), displaces paxillin from focal adhesions, and reduces Arf6 activity explained the molecular basis for Rac3's anti-adhesive function through a GIT1–Arf6 axis.

    Evidence Co-IP, siRNA, Arf6/ARNO rescue of spreading, GTPase activity assays

    PMID:19494130

    Open questions at the time
    • Structural basis of βPix-independent GIT1 binding unknown
    • Whether GIT1–Arf6 axis operates in neuronal contexts not tested
  9. 2011 High

    Rac3 was identified as an isoform-specific negative regulator of autophagy (Rac1/Rac2 depletion had no effect), and concurrent studies showed Rac1/Rac3 double knockout impairs hippocampal mossy cell migration without affecting proliferation, broadening Rac3's CNS functions beyond motor circuits.

    Evidence Isoform-specific siRNA with Rac3 rescue in autophagy assays; conditional Rac1/Rac3 double KO with BrdU migration tracing in hippocampus

    PMID:21852230 PMID:21949760

    Open questions at the time
    • Autophagy regulation mechanism (direct target of Rac3 in autophagy pathway) not identified
    • Individual contribution of Rac3 versus Rac1 in mossy cell migration not separated
  10. 2014 High

    Identification of FBXL19 as the E3 ligase mediating K166-specific polyubiquitination and proteasomal degradation of Rac3 established the first post-translational degradation mechanism for this GTPase, linking it to TGFβ1-induced EMT.

    Evidence Co-IP, ubiquitination assay with K166R mutant, FBXL19 domain truncations, E-cadherin assay in esophageal cancer cells

    PMID:24684802

    Open questions at the time
    • Whether FBXL19-mediated Rac3 degradation operates in normal physiology (beyond cancer) unknown
    • Regulation of FBXL19 activity toward Rac3 not explored
  11. 2017 High

    A Rac3-specific FRET biosensor demonstrated that Vav2, recruited by phospho-cortactin, activates Rac3 specifically at invadopodia to drive matrix degradation and invasion; separately, Rac3 was linked to p38 MAPK–dependent EMT in lung cancer and to ER stress–autophagy through HSPA5 interaction.

    Evidence FRET biosensor at invadopodia, Vav2/Rac3 epistasis rescue, p38 MAPK inhibitor phenocopy in lung cancer cells, Rac3–HSPA5 Co-IP with ATF4/DDIT4 epistasis

    PMID:28356423 PMID:28534368 PMID:28900489

    Open questions at the time
    • Whether ER stress–autophagy axis operates independently of the known autophagy function awaits confirmation
    • HSPA5 interaction needs independent validation
  12. 2018 Medium

    Identification of de novo activating RAC3 missense variants in patients with severe intellectual disability and brain malformations established RAC3 as a neurodevelopmental disease gene (NEDBAF), though initial evidence was primarily in silico.

    Evidence Genome sequencing of affected individuals, in silico structural modeling, international data-sharing

    PMID:30293988

    Open questions at the time
    • No direct biochemical assays of the variants performed in this study
    • Genotype–phenotype correlation across variant classes not yet defined
  13. 2021 Medium

    Genetic epistasis in peripheral nerve revealed that Rac3 opposes Rac1 during Schwann cell myelination: Rac3 deletion rescued axonal sorting, myelination, and PAK1 phosphorylation defects caused by Rac1 loss, extending the antagonistic Rac1/Rac3 paradigm beyond adhesion to myelination.

    Evidence Rac1 conditional KO × Rac3 global KO mice, radial sorting histology, PAK1 phosphorylation immunoblot

    PMID:33812927

    Open questions at the time
    • Mechanism by which Rac3 inhibits myelination-promoting PAK1 signals not determined
    • Single lab; no independent replication
  14. 2022 High

    Comprehensive biochemical and in vivo characterization of multiple RAC3 disease variants demonstrated that gain-of-function mutations in Switch I/II regions cause cortical neuron migration defects through PAK1 hyperactivation (rescued by dominant-negative PAK1), while Rac3 also promotes dendritic spine enlargement with functional synapse formation, and negatively regulates autophagy via PI3K/AKT/mTOR.

    Evidence GTPase/effector assays, in utero electroporation in mouse cortex, dominant-negative PAK1 rescue, double-KO neuron re-expression spine analysis, shRAC3 with mTOR modulation in vivo xenograft

    PMID:31369617 PMID:35595279 PMID:35847878 PMID:35851598

    Open questions at the time
    • Whether PAK1 rescue applies to all variant classes remains open
    • Structural basis for variant-specific effector preferences not resolved
  15. 2024 High

    The p.R66W variant revealed a distinct signaling-competent-but-transcriptionally-inactive class: it binds PAK1/MLK2/N-WASP yet fails to activate SRF/NF-κB/AP1 reporters, still causing cortical migration and axon defects, demonstrating that effector binding alone does not predict transcriptional output or disease severity.

    Evidence GDP/GTP exchange, GTP hydrolysis, effector pulldowns, luciferase reporters, in utero electroporation

    PMID:39682779

    Open questions at the time
    • Molecular basis for dissociation between effector binding and transcriptional activation unknown
    • Whether p.R66W acts through a novel signaling branch untested
  16. 2025 High

    Discovery of the p.T17R signaling-deficient allele (minimal effector binding, no transcriptional activation) and the GAP-resistant p.N92K variant expanded the mechanistic spectrum of RAC3 disease variants; separately, RAC3 was implicated in prion-induced ferroptosis through lipid/ROS modulation.

    Evidence Biochemical exchange/hydrolysis assays, effector pulldowns, in utero electroporation for T17R and N92K; RAC3 knockdown with ferroptosis markers in CJD patient cortex

    PMID:40015633 PMID:40562790 PMID:41090727

    Open questions at the time
    • How a signaling-deficient allele (T17R) still disrupts migration is mechanistically unresolved
    • RAC3's role in ferroptosis requires dissection of direct lipid-metabolic targets

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for variant-specific effector engagement and transcriptional output divergence, the direct molecular target(s) through which RAC3 suppresses autophagy and modulates ferroptosis, the mechanism underlying Rac3's antagonism of Rac1 in myelination and adhesion, and whether therapeutic targeting of PAK1 can ameliorate NEDBAF-associated neurodevelopmental defects.
  • No high-resolution structure of RAC3 with effectors or GAPs
  • No therapeutic rescue of NEDBAF in animal models
  • Direct autophagy/ferroptosis targets of RAC3 unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 5 GO:0098772 molecular function regulator activity 3
Localization
GO:0005886 plasma membrane 3 GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-1266738 Developmental Biology 5 R-HSA-112316 Neuronal System 4 R-HSA-1643685 Disease 4 R-HSA-9612973 Autophagy 3
Partners
BCRCIB1FBXL19GIT1HSPA5NRBN1PAK1VAV2

Evidence

Reading pass · 39 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 RAC3 (Rho GTPase) was cloned as a novel third Rac family member; Rac3 protein is a functional GTPase whose GTPase activity is regulated by Bcr. The C-terminal domain is distinct from Rac1/2 and associated with subcellular localization and binding to specific regulators. When constitutively activated, Rac3 efficiently stimulates the c-Jun N-terminal kinase (JNK) signaling pathway. Rac3 protein levels are serum-inducible. Molecular cloning, GTPase activity assay, JNK pathway reporter assays, immunoblotting with serum stimulation The Journal of biological chemistry High 9252344
2000 Endogenous Rac3 is hyperactive in highly proliferative human breast cancer cell lines and tumor tissues, resulting from its distinct membrane localization and altered regulatory factors affecting guanine nucleotide state. Active Rac3 drives persistent kinase activity of two PAK isoforms and JNK via two separate pathways, and only the Rac3–PAK pathway (not JNK) is critical for DNA synthesis. GTPase activity pulldown assays, dominant-negative transfection of Rac3 and PAK1 fragments, DNA synthesis assays in breast cancer cell lines Proceedings of the National Academy of Sciences of the United States of America High 10618392
2001 CIB (calcium- and integrin-binding protein), which binds the alpha(IIb)beta(3) fibrinogen receptor, interacts exclusively with activated (GTP-bound, V12) Rac3 but not Rac1 or Rac2. Binding requires the C-terminal end of Rac3 and Rac3 membrane localization. alpha(IIb)beta(3)-mediated adhesion on fibrinogen specifically increases endogenous GTP-bound Rac3 (but not Rac1), and co-expression of V12Rac3 with CIB stimulates integrin-mediated adhesion and spreading. Co-immunoprecipitation, GST pulldown, co-localization by immunofluorescence, GTPase pulldown assay, adhesion/spreading assays The Journal of biological chemistry High 11756406
2002 NRBP (a protein with a kinase-homology domain) was identified as a Rac3-interacting protein. NRBP forms a complex specifically with activated Rac3 (not GDP-bound), and the two co-localize to endomembranes and cell periphery lamellipodia. Overexpression of NRBP causes redistribution of the Golgi marker p58, suggesting NRBP functions in subcellular trafficking directed partly through Rac3 interaction. Yeast two-hybrid screen, Co-immunoprecipitation in COS cells, immunocytochemistry co-localization International journal of molecular medicine Medium 11956649
2003 Rac3 causes transformation (focus formation and anchorage-independent growth) and membrane ruffling in fibroblasts, and activates c-Jun transcriptional activity. Geranylgeranylation is required for Rac3 biological activity; COOH-terminal mutants that accept farnesyl instead of geranylgeranyl retain signaling to c-Jun and membrane ruffling, demonstrating that isoprenoid switching does not alter function. GGTIs inhibit both membrane-ruffling and transforming activities of wild-type Rac1 and Rac3, while farnesylated versions are resistant, identifying Rac1 and Rac3 as physiological GGTI targets. COOH-terminal lipid modification mutants, GGTI treatment, transformation assays (focus formation, soft agar), membrane ruffling assays, c-Jun luciferase reporter Cancer research High 14633727
2003 Rac3 protein is differentially expressed during mouse brain development, peaking at times of neuronal maturation and synaptogenesis, with distinct subcellular distribution compared to Rac1. Rac3 co-localizes with actin filaments and with terminal portions of calbindin-positive Purkinje cell axons in deep cerebellar nuclei, implicating Rac3 in actin-mediated remodeling of Purkinje cell neuritic terminals during synaptogenesis. Rac3-specific antibody immunohistochemistry/immunofluorescence, subcellular co-localization with actin, pre/post-synaptic markers, GFAP, and calbindin The European journal of neuroscience Medium 14622142
2003 Constitutively active V12Rac3 expressed in mammary epithelium under the MMTV promoter elevates Pak1 phosphorylation. Sustained Rac3 activation leads to impaired lactational differentiation, failure of postlactational involution (associated with decreased apoptosis and increased p38 MAPK phosphorylation after 5 days), and persistent epithelial islands and ductal abnormalities months postpartum. Transgenic mouse model (MMTV-V12Rac3), immunoblotting for Pak1 phosphorylation and p38 MAPK phosphorylation, apoptotic index, histological analysis Cells, tissues, organs Medium 14605486
2005 Rac3-mediated transformation requires multiple effector pathways. Effector domain mutants (EDMs) of Rac3 reveal that membrane ruffling and focus formation are retained by all EDMs tested, but anchorage-independent growth requires N43D specifically. Rac3 activates phospholipase Cβ2 signaling to SRF and also activates cyclin D1 transcription (the only pathway correlating with anchorage-independent growth). Notably, Rac3 binds poorly to MLK2 and MLK3 (known Rac1 effectors), distinguishing Rac3 effector usage from Rac1. Effector domain mutants, focus formation, soft agar transformation assays, luciferase reporter assays (SRF, AP-1, E2F, NF-κB), GST pulldown for effector binding Cancer research High 16267012
2005 Rac3 knockout mice are viable and fertile with no obvious developmental defects, but show specific behavioral differences including superior motor coordination and motor learning on the rotarod, demonstrating a non-redundant role for Rac3 in the developing nervous system that is not compensated by Rac1. Gene targeting (knockout mice), rotarod motor learning test, histological and immunohistological analysis Molecular and cellular biology High 15964829 15964830
2005 In BCR/ABL P190 transgenic lymphoblastic leukemia, activated Rac3 (but not Rac1 or Rac2) is detectable in malignant precursor B-lineage lymphoblasts. Vav1 (a Rac GEF) is constitutively tyrosine phosphorylated in these cells. In female P190 BCR/ABL transgenic mice lacking rac3, average survival was prolonged, demonstrating a stimulatory role for Rac3 in BCR/ABL-driven leukemia in vivo. Rac3 knockout mice crossed with BCR/ABL transgenic, GTP-Rac3 pulldown assay, survival analysis Molecular and cellular biology High 15964830
2005 siRNA-mediated depletion of Rac3 strongly inhibits SNB19 glioblastoma and BT549 breast carcinoma cell invasion but does not affect lamellipodia formation and has only minor effects on migration and proliferation, revealing a distinct role for Rac3 in invasion compared to Rac1 (which controls lamellipodia, migration, and invasion). siRNA knockdown (Rac1 and Rac3 specific), invasion assay (Matrigel), lamellipodia formation assay, migration assay, proliferation/survival assay Oncogene High 16027728
2005 Dominant-active Rac1 or Rac3 increases invasive and motile phenotype of low-metastatic breast cancer cells; dominant-negative Rac1 or Rac3 decreases invasion and migration of highly metastatic cells. Endogenous Rac activity (measured by PAK-PBD pulldown) directly correlates with increasing metastatic potential in MDA-MB-435 variant panel. Stable expression of dominant-active/negative Rac isoforms, p21-binding domain PAK pulldown assay, in vitro adhesion/migration/invasion assays Breast cancer research : BCR Medium 16280046
2006 Neurabin I (neuronal F-actin binding protein) is a direct Rac3-interacting molecule identified by yeast two-hybrid. Neurabin I co-partitions and co-localizes with Rac3 at neurite growth cones, inducing Neurabin I association to the cytoskeleton. Antisense knockdown of Neurabin I abolishes Rac3-induced neuritogenesis, which is rescued by exogenous Neurabin I but not by a Neurabin I mutant lacking the Rac3-binding domain, demonstrating that Neurabin I mediates Rac3-induced neuritogenesis by anchoring Rac3 to growth cone F-actin. Yeast two-hybrid, biochemical co-fractionation, immunofluorescence co-localization, antisense oligonucleotide knockdown, rescue with binding-domain mutant Molecular biology of the cell High 16525025
2007 Rac1 and Rac3 have opposing functions in neuronal N1E-115 cells: Rac1 depletion causes decreased cell-matrix adhesions and cell rounding, while Rac3 depletion induces stronger adhesions and increased neurite-like protrusion outgrowth. Rac1 is mainly at the plasma membrane; Rac3 is predominantly in the perinuclear region. Residues 185–187 in the C-terminal polybasic region are responsible for both the opposite phenotypes and the different intracellular localizations. Rac3's opposing function acts through disruption of integrin-mediated cell-matrix adhesions, independently of RhoA signaling. siRNA knockdown (isoform-specific), overexpression, C-terminal chimeric mutants, immunofluorescence localization, cell morphology/adhesion assays Journal of cell science High 17244648
2009 Both Rac1 and Rac3 interact with GIT1 (an Arf-GAP protein), but via different mechanisms: Rac1-GIT1 interaction requires βPix, while Rac3-GIT1 interaction does not. Rac3 expression severely attenuates the GIT1–paxillin interaction, causing defective paxillin distribution and focal adhesion formation. In Rac3-expressing cells, Arf6 activity is strongly reduced and GIT1's Arf6-GAP activity is required for Rac3 downstream signaling; expression of wild-type Arf6 or the Arf6-GEF ARNO rescues cell spreading in Rac3-expressing cells. Co-immunoprecipitation, siRNA knockdown, overexpression of Arf6/ARNO, immunofluorescence for paxillin/focal adhesions, GTPase activity assays Journal of cell science High 19494130
2011 Rac3 GTPase is a negative regulator of autophagy. siRNA knockdown of Rac3 (but not closely related Rac1 or Rac2) induces autophagy. Ectopic expression of Rac3 rescues cells from autophagy and cell death induced by isoprenylcysteine carboxylmethyltransferase (Icmt) inhibition, demonstrating isoform-specific autophagy regulation. siRNA knockdown (Rac1, Rac2, Rac3 specific), Icmt inhibitor treatment, autophagy assays (LC3 puncta, autophagy flux), ectopic Rac3 rescue experiments The Journal of biological chemistry High 21852230
2011 Rac1 and Rac3 GTPases regulate the migration of hilar mossy cell precursors during hippocampal development. Double knockout of Rac1 and Rac3 results in loss of mossy cells evident at postnatal day 8, with reduced presynaptic input but no increase in apoptosis. BrdU labeling revealed a defect in migration of immature mossy cells to the dorsal hilus, rather than defective proliferation. Conditional Rac1 and Rac3 double knockout mice, BrdU labeling at E12.5, immunohistochemistry for mossy cell markers, synaptogenesis markers, apoptosis assays PloS one Medium 21949760
2013 In invasive MDA-MB-231 breast cancer cells, Rac3 depletion reduces invasion (40%) and adhesion to collagen (84%), and increases TNF-induced apoptosis (72%). The Rac3-dependent aggressiveness operates through a Rac3/ERK-2/NF-κB signaling pathway responsible for MMP-9, IL-6, IL-8 and GRO secretion. This pathway is non-functional in non-invasive MCF-7 cells due to low NF-κB subunit expression. Anti-Rac3 siRNA knockdown, invasion assay, adhesion assay, apoptosis assay, western blotting for ERK-2/NF-κB activation, cytokine secretion profiling BMC cancer Medium 23388133
2014 FBXL19 (an F-box protein) interacts with Rac3, polyubiquitinates it, and promotes its proteasomal degradation. Lysine 166 within Rac3 was identified as the ubiquitination acceptor site. The C-terminus of FBXL19 is required for Rac3 interaction and ubiquitination. Rac3 plays a critical role in TGFβ1-induced E-cadherin downregulation in esophageal cancer cells; FBXL19 overexpression attenuates this effect. Co-immunoprecipitation, immunoblotting for Rac3 stability, ubiquitination assay with K166 mutant, FBXL19 truncation mutants, siRNA knockdown, E-cadherin immunostaining Molecular cancer High 24684802
2015 Rac1 and Rac3 have independent roles in the formation of hippocampal GABAergic circuits. Conditional Rac1 knockout causes greater generalized hyperactivity, cognitive impairment, higher excitability, and reduced spontaneous inhibitory currents in CA pyramidal neurons compared to Rac3 full KO. Both knockouts cause similar reduction of parvalbumin-positive inhibitory terminals, but cannabinoid receptor-1-positive terminals are strongly increased only in Rac1-depleted CA1, and an antagonist for cannabinoid receptors partially rescues inhibitory current reduction in Rac1 but not Rac3 mutants. Conditional Rac1 KO and full Rac3 KO mice, behavioral testing, electrophysiology (inhibitory currents in pyramidal cells), immunohistochemistry for interneuron markers, pharmacological rescue with cannabinoid receptor antagonist Cerebral cortex High 26582364
2017 Phosphorylated cortactin recruits the Rho-GEF Vav2 via its SH2 domain binding to phosphotyrosines Y421 and Y466 of cortactin (but not Y482). Vav2 is required at invadopodia for actin polymerization, matrix degradation and invasive migration. Using a Rac3-specific biosensor, Vav2 was shown to activate Rac3 specifically at invadopodia. Rac3 knockdown reduces matrix degradation by invadopodia, while constitutively active Rac3 rescues invadopodium function in Vav2-knockdown cells. SH2 domain screen, Vav2 SH2 domain phosphopeptide binding assay, invadopodium maturation assay, FRET-based Rac3 biosensor, siRNA knockdown of Vav2 and Rac3, rescue with constitutively active Rac3 Molecular biology of the cell High 28356423
2017 Rac3 knockdown in lung adenocarcinoma cells (A549 and H1299) inhibits cell invasion, migration, and epithelial-to-mesenchymal transition (EMT). These effects are mediated via the p38 MAPK pathway: Rac3 silencing decreases p38 MAPK activity, and the p38 MAPK inhibitor LY2228820 phenocopies Rac3 knockdown (increased E-cadherin, decreased vimentin). The p38 MAPK inhibitor blocks Rac3-induced invasion and migration. Lentivirus-mediated shRNA knockdown, PathScan intracellular signaling array, western blot, p38 MAPK pharmacological inhibitor (LY2228820), invasion/migration assays Journal of Cancer Medium 28900489
2018 De novo monoallelic missense variants in RAC3 (Rho GTPase) cause a novel neurodevelopmental syndrome with severe intellectual disability and brain malformations. In silico protein modeling and prior experimental data support a constitutively activating (transforming) effect for each of three variants identified. All variants correspond to residues observed as somatic mutations in cancer databases. Genome sequencing, in silico protein modeling, international data-sharing, functional assessment Genetics in medicine Medium 30293988
2019 Rac1 and Rac3 GTPases are co-expressed in developing hippocampal neurons. Overexpression of either GTPase in wild-type neurons increases dendritic spine density. Re-expression of either Rac1 or Rac3 alone in double-knockout neurons restores spinogenesis. Rac1 is more efficient at inducing formation of mature spines, while Rac3 more efficiently promotes spine enlargement, with enlarged spines forming morphological synapses identified by juxtaposed pre/post-synaptic markers. Overexpression and re-expression in double-KO hippocampal cultures, dendritic spine quantification (density, size, morphology), synaptic marker immunostaining PloS one Medium 31369617
2020 RAC3 (Rho GTPase) promotes bladder cancer cell proliferation, migration, and invasion by activating JAK/STAT signaling. RAC3 upregulates PYCR1, which is positively correlated with RAC3 expression; RAC3 overexpression activates JAK/STAT signaling via PYCR1 axis. siRNA/overexpression, MTT/colony formation/Transwell assays, western blotting for JAK/STAT activation, RT-qPCR Frontiers in molecular biosciences Low 33062641
2021 Rac3 protein in developing hippocampal neurons is distributed mainly in the cytoplasm but also present in axons, dendrites, and partially at synapses, as confirmed by biochemical fractionation and immunofluorescence in brain slices. In cerebral cortex at postnatal days 2 and 18, Rac3 is distributed strongly in axons and moderately in cytoplasm. Immunoblotting, biochemical synaptosome fractionation, immunofluorescence in primary cultured neurons and brain slices Developmental neuroscience Medium 34839287
2022 De novo RAC3 variants (p.G12R, p.G60D, p.E62del, p.D63N, p.Y64C, p.K116N, plus previously reported variants) cause neurodevelopmental disorder with cortical malformations. In vitro analyses showed all variants are biochemically and biologically active with variable affinity to downstream effectors including PAK1. In utero electroporation in mouse embryonic brain with Switch II region variants (p.Q61L, p.E62del, p.D63N, p.Y64C) caused defects in cortical neuron morphology and migration, with cluster formation during corticogenesis. Defective migration by p.E62del, p.D63N, and p.Y64C (but not p.Q61L) was rescued by dominant-negative PAK1, placing PAK1 downstream of these variants. In vitro GTPase/effector binding assays, in utero electroporation in mouse embryonic brain, cortical neuron migration assays, dominant-negative PAK1 rescue Brain : a journal of neurology High 35851598
2022 RAC3 (Rho GTPase) knockdown in bladder cancer cells activates PI3K/AKT/mTOR-mediated autophagy and inhibits proliferation and migration in vitro and in vivo. Autophagy inhibitor 3-MA partially rescues migration and proliferation defects from RAC3 knockdown. Modulation of mTOR enhances or impairs autophagy accordingly, with shRAC3-mediated migration defects exacerbated by mTOR inhibition and rescued by mTOR activation. KD/OE cell lines, in vivo xenograft, autophagy assays, PI3K/AKT/mTOR pathway western blotting, mTOR modulation, 3-MA treatment Frontiers in oncology Medium 35847878
2022 The novel RAC3 gain-of-function variant p.F28S shows spontaneously increased intrinsic GTP/GDP-exchange activity and binds downstream effectors PAK1 and MLK2. It suppresses hippocampal neuron differentiation and causes cell rounding with lamellipodia in vitro. In vivo in utero electroporation shows migration defects and axon growth delay in cortex. Defective migration is rescued by dominant-negative PAK1 but not MLK2, placing PAK1 as the critical downstream effector. Intrinsic nucleotide exchange assay, effector pulldown, primary hippocampal neuron morphology, in utero electroporation, PAK1 and MLK2 dominant-negative rescue Journal of medical genetics High 35595279
2023 METTL3 in NSCLC cells (induced by CAF-secreted VEGFA) increases m6A modification of RAC3 mRNA, resulting in increased RAC3 mRNA stability and translation. RAC3 protein is then responsible for CAF-promoted cell migration and invasion via the AKT/NF-κB pathway. METTL3 knockdown suppresses tumor growth in vivo. m6A methylation assay, mRNA stability assay, siRNA knockdown, western blotting for RAC3 and AKT/NF-κB, in vivo xenograft International journal of biological sciences Medium 37056933
2024 The RAC3 variant p.R66W shows modestly enhanced intrinsic GDP/GTP exchange activity and inhibitory effect on GTP hydrolysis. It interacts with downstream effectors PAK1, MLK2, and N-WASP but fails to activate SRF-, AP1-, and NF-κB-mediated transcription. Overexpression impairs primary hippocampal neuron differentiation and, by in utero electroporation, causes cortical neuron migration and axonal elongation defects — demonstrating variant-specific mechanisms. Biochemical GDP/GTP exchange and hydrolysis assays, effector pulldown, luciferase reporter assays, primary neuron morphology, in utero electroporation Cells High 39682779
2025 RAC3 (Rho GTPase) facilitates prion-induced ferroptosis. Depletion of RAC3 is observed selectively in pathologically afflicted cortices of CJD patients. RAC3 synergistically modulates lipids and reactive oxygen species that drive ferroptosis susceptibility in the context of prion disease. RAC3 knockdown, ferroptosis markers, CJD patient cortex analysis, lipid peroxidation assays Nature communications Medium 40562790
2025 The RAC3 variant p.N92K (located outside canonical functional domains) is resistant to GAP-mediated GTP hydrolysis but remains responsive to GEF activation and capable of binding PAK1, MLK2, and Rho-kinase 1. It activates SRF, NF-κB, and AP1 gene expression. Structural analysis shows N92K disrupts GAP interactions while preserving GEF and effector interactions. In vivo expression in embryonic cortical neurons causes migration defects and periventricular clustering, as well as impaired axon elongation. Biochemical GAP assay, GEF activation assay, effector pulldown, luciferase reporter (SRF/NF-κB/AP1), structural/in silico modeling, in utero electroporation, cortical neuron morphology The Journal of biological chemistry High 40015633
2025 The RAC3 variant p.T17R shows markedly increased GDP/GTP exchange with preference for GDP binding and undetectable GTP hydrolysis. It exhibits minimal binding to canonical RAC effectors (PAK1, MLK2, N-WASP) and fails to activate SRF-, NF-κB-, or AP1-dependent transcription, behaving as a signaling-deficient allele. In vivo in utero electroporation shows delayed cortical neuron migration, impaired axon extension, and reduced dendritic arborization, with the fetus presenting corpus callosum agenesis, microcephaly, and multisystem defects. GDP/GTP exchange assay, GTP hydrolysis assay, effector pulldown, luciferase reporters, primary hippocampal neuron morphology, in utero electroporation Cells High 41090727
2021 In Schwann cells, Rac3 has an opposing function to Rac1 during peripheral myelination. Global deletion of Rac3 alleviates developmental defects on axonal sorting and hypomyelination caused by Schwann cell-specific Rac1 ablation. Rac3 deletion also reverses the arrest of Schwann cells at the Oct6+ immature stage and ameliorates defects in PAK1 phosphorylation observed in Rac1-deficient mice, consistent with Rac3 disrupting PAK1-GIT1-paxillin signaling. Conditional Rac1 and global Rac3 knockout mice, radial sorting analysis, myelination histology, Oct6 immunostaining, PAK1 phosphorylation western blot Neuroscience letters Medium 33812927
2025 CCR7 tyrosine phosphorylation at invadopodia directs recruitment of Vav2, which activates Rac3 to promote cancer cell invasion across lymphatic endothelium and lymph node metastasis. CCR7 localizes to invadopodia, and Tks5-positive invadopodia remodel lymphatic endothelial junctions. Loss of Tks5 impairs invasion across lymphatic endothelium and reduces lymph node and lung metastasis in a mouse breast cancer model. CCR7 invadopodium localization, Vav2 recruitment assay, Rac3 activation assay, Tks5 loss-of-function, in vivo mouse breast cancer model, lymph node/lung metastasis quantification bioRxivpreprint Medium bio_10.1101_2025.10.15.682688
2024 SETD8 inhibits apoptosis and ferroptosis in Ewing's sarcoma through a YBX1/RAC3 axis: SETD8 facilitates nuclear translocation of YBX1, which transcriptionally upregulates RAC3. SETD8 knockdown induces apoptosis and ferroptosis in ES cells and suppresses tumorigenesis in vivo. RNA-seq, mass spectrometry proteomics, SETD8 inhibitor (UNC0379) and siRNA, YBX1 nuclear translocation assay, RAC3 expression analysis, apoptosis/ferroptosis assays, xenograft Cell death & disease Medium 38987564
2024 KLF1 transcription factor activates RAC3 transcription (confirmed by dual-luciferase and ChIP assays). RAC3 is enriched in the fatty acid synthesis pathway and correlates with FASN expression. RAC3 overexpression promotes cisplatin resistance in T24/DDP bladder cancer cells via FASN-mediated fatty acid synthesis; FASN inhibitor Orlistat mitigates this effect. Dual-luciferase reporter, ChIP assay, GSEA, western blot for FASN/DGAT2, fatty acid/triglyceride quantification, CCK-8, colony formation American journal of men's health Medium 39376007
2017 Inhibition of Rac3 in human lung cancer cells leads to acetylation of HSPA5 (BiP/GRP78), causing its dissociation from EIF2AK3 (PERK) on the ER membrane, activating ER stress response. ER stress then activates ATF4 and upregulates DDIT4 (REDD1), which inhibits the mTOR signaling pathway and induces autophagy. Co-immunoprecipitation revealed Rac3 interacts with HSPA5. siRNA knockdown, laser confocal microscopy (EGFP-MAP1LC3 puncta), immunoblotting, ATF4/DDIT4 siRNA and overexpression, co-immunoprecipitation of Rac3 and HSPA5, autophagy inhibitors Journal of B.U.ON. Medium 28534368

Source papers

Stage 0 corpus · 108 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 A CBP integrator complex mediates transcriptional activation and AP-1 inhibition by nuclear receptors. Cell 1894 8616895
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1997 AIB1, a steroid receptor coactivator amplified in breast and ovarian cancer. Science (New York, N.Y.) 1396 9252329
2006 A probability-based approach for high-throughput protein phosphorylation analysis and site localization. Nature biotechnology 1336 16964243
1998 An orphan nuclear receptor activated by pregnanes defines a novel steroid signaling pathway. Cell 1284 9489701
1997 Nuclear receptor coactivator ACTR is a novel histone acetyltransferase and forms a multimeric activation complex with P/CAF and CBP/p300. Cell 1255 9267036
2009 A census of human transcription factors: function, expression and evolution. Nature reviews. Genetics 1191 19274049
2004 Large-scale characterization of HeLa cell nuclear phosphoproteins. Proceedings of the National Academy of Sciences of the United States of America 1159 15302935
1997 The transcriptional co-activator p/CIP binds CBP and mediates nuclear-receptor function. Nature 1099 9192892
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2018 High-Density Proximity Mapping Reveals the Subcellular Organization of mRNA-Associated Granules and Bodies. Molecular cell 580 29395067
1999 Regulation of hormone-induced histone hyperacetylation and gene activation via acetylation of an acetylase. Cell 543 10490106
1998 Transcription factor-specific requirements for coactivators and their acetyltransferase functions. Science (New York, N.Y.) 540 9445475
2015 Progesterone receptor modulates ERα action in breast cancer. Nature 532 26153859
1995 Human type II receptor for bone morphogenic proteins (BMPs): extension of the two-kinase receptor model to the BMPs. Molecular and cellular biology 506 7791754
1997 RAC3, a steroid/nuclear receptor-associated coactivator that is related to SRC-1 and TIF2. Proceedings of the National Academy of Sciences of the United States of America 493 9238002
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2000 The steroid receptor coactivator SRC-3 (p/CIP/RAC3/AIB1/ACTR/TRAM-1) is required for normal growth, puberty, female reproductive function, and mammary gland development. Proceedings of the National Academy of Sciences of the United States of America 432 10823921
2001 Regulation of histone acetylation and transcription by INHAT, a human cellular complex containing the set oncoprotein. Cell 413 11163245
2006 Mir-17-5p regulates breast cancer cell proliferation by inhibiting translation of AIB1 mRNA. Molecular and cellular biology 412 16940181
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1996 Normalization and subtraction: two approaches to facilitate gene discovery. Genome research 401 8889548
2002 Mutual synergistic folding in recruitment of CBP/p300 by p160 nuclear receptor coactivators. Nature 366 11823864
2000 AIB1 is a conduit for kinase-mediated growth factor signaling to the estrogen receptor. Molecular and cellular biology 359 10866661
2006 Hematopoiesis controlled by distinct TIF1gamma and Smad4 branches of the TGFbeta pathway. Cell 318 16751102
1997 TRAM-1, A novel 160-kDa thyroid hormone receptor activator molecule, exhibits distinct properties from steroid receptor coactivator-1. The Journal of biological chemistry 316 9346901
2013 Endogenous purification reveals GREB1 as a key estrogen receptor regulatory factor. Cell reports 307 23403292
2001 Synergistic enhancement of nuclear receptor function by p160 coactivators and two coactivators with protein methyltransferase activities. The Journal of biological chemistry 297 11050077
2000 The opposing transcriptional activities of the two isoforms of the human progesterone receptor are due to differential cofactor binding. Molecular and cellular biology 290 10757795
2002 T0070907, a selective ligand for peroxisome proliferator-activated receptor gamma, functions as an antagonist of biochemical and cellular activities. The Journal of biological chemistry 276 11877444
1997 Characterization of RAC3, a novel member of the Rho family. The Journal of biological chemistry 210 9252344
2005 Roles of the Rac1 and Rac3 GTPases in human tumor cell invasion. Oncogene 202 16027728
2000 Endogenous, hyperactive Rac3 controls proliferation of breast cancer cells by a p21-activated kinase-dependent pathway. Proceedings of the National Academy of Sciences of the United States of America 202 10618392
2005 Rac1 and Rac3 isoform activation is involved in the invasive and metastatic phenotype of human breast cancer cells. Breast cancer research : BCR 106 16280046
2000 RAC-3 is a NF-kappa B coactivator. FEBS letters 103 11094166
2005 Generation and characterization of Rac3 knockout mice. Molecular and cellular biology 98 15964829
2012 The nuclear cofactor RAC3/AIB1/SRC-3 enhances Nrf2 signaling by interacting with transactivation domains. Oncogene 94 22370642
2013 Rac3 induces a molecular pathway triggering breast cancer cell aggressiveness: differences in MDA-MB-231 and MCF-7 breast cancer cell lines. BMC cancer 93 23388133
2003 The MN1 oncoprotein synergizes with coactivators RAC3 and p300 in RAR-RXR-mediated transcription. Oncogene 73 12569362
2003 Differential distribution of Rac1 and Rac3 GTPases in the developing mouse brain: implications for a role of Rac3 in Purkinje cell differentiation. The European journal of neuroscience 72 14622142
2001 The small GTPase Rac3 interacts with the integrin-binding protein CIB and promotes integrin alpha(IIb)beta(3)-mediated adhesion and spreading. The Journal of biological chemistry 58 11756406
2014 F-box protein complex FBXL19 regulates TGFβ1-induced E-cadherin down-regulation by mediating Rac3 ubiquitination and degradation. Molecular cancer 55 24684802
2003 Rac1 and Rac3 are targets for geranylgeranyltransferase I inhibitor-mediated inhibition of signaling, transformation, and membrane ruffling. Cancer research 52 14633727
2007 The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action. Oncogene 49 17968310
2005 Generation of rac3 null mutant mice: role of Rac3 in Bcr/Abl-caused lymphoblastic leukemia. Molecular and cellular biology 46 15964830
2022 Variant-specific changes in RAC3 function disrupt corticogenesis in neurodevelopmental phenotypes. Brain : a journal of neurology 45 35851598
2020 RAC3 Promotes Proliferation, Migration and Invasion via PYCR1/JAK/STAT Signaling in Bladder Cancer. Frontiers in molecular biosciences 44 33062641
2007 Rac1 and Rac3 have opposing functions in cell adhesion and differentiation of neuronal cells. Journal of cell science 42 17244648
2018 De novo missense variants in RAC3 cause a novel neurodevelopmental syndrome. Genetics in medicine : official journal of the American College of Medical Genetics 40 30293988
2017 Phosphorylated cortactin recruits Vav2 guanine nucleotide exchange factor to activate Rac3 and promote invadopodial function in invasive breast cancer cells. Molecular biology of the cell 39 28356423
2017 Rac3 Regulates Cell Invasion, Migration and EMT in Lung Adenocarcinoma through p38 MAPK Pathway. Journal of Cancer 37 28900489
2019 The Rac3 GTPase in Neuronal Development, Neurodevelopmental Disorders, and Cancer. Cells 36 31514269
2006 Regulation of Nrf2 transactivation domain activity by p160 RAC3/SRC3 and other nuclear co-regulators. Journal of biochemistry and molecular biology 35 16756760
2011 A role for Rac3 GTPase in the regulation of autophagy. The Journal of biological chemistry 33 21852230
2023 Cancer-associated fibroblasts promote migration and invasion of non-small cell lung cancer cells via METTL3-mediated RAC3 m6A modification. International journal of biological sciences 32 37056933
2011 RAC3 is a pro-migratory co-activator of ERα. Oncogene 31 21217774
2007 RAC3 down-regulation sensitizes human chronic myeloid leukemia cells to TRAIL-induced apoptosis. FEBS letters 30 17927986
2015 Loss of Either Rac1 or Rac3 GTPase Differentially Affects the Behavior of Mutant Mice and the Development of Functional GABAergic Networks. Cerebral cortex (New York, N.Y. : 1991) 28 26582364
2017 RAC3 influences the chemoresistance of colon cancer cells through autophagy and apoptosis inhibition. Cancer cell international 26 29209153
2002 Interaction of the small GTPase Rac3 with NRBP, a protein with a kinase-homology domain. International journal of molecular medicine 26 11956649
2022 RAC3 Inhibition Induces Autophagy to Impair Metastasis in Bladder Cancer Cells via the PI3K/AKT/mTOR Pathway. Frontiers in oncology 25 35847878
2022 Gain-of-function p.F28S variant in RAC3 disrupts neuronal differentiation, migration and axonogenesis during cortical development, leading to neurodevelopmental disorder. Journal of medical genetics 24 35595279
2009 Rac3 inhibits adhesion and differentiation of neuronal cells by modifying GIT1 downstream signaling. Journal of cell science 24 19494130
2007 Hyperactivity and novelty-induced hyperreactivity in mice lacking Rac3. Behavioural brain research 24 17889944
2003 Targeted expression of activated Rac3 in mammary epithelium leads to defective postlactational involution and benign mammary gland lesions. Cells, tissues, organs 22 14605486
1997 Structure and chromosomal assignment to 22q12 and 17qter of the ras-related Rac2 and Rac3 human genes. Genomics 21 9299243
2019 Rac1 and Rac3 GTPases differently influence the morphological maturation of dendritic spines in hippocampal neurons. PloS one 20 31369617
2005 Expression of Rac3 in human brain tumors. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 20 15993075
2000 The small GTPase RAC3 gene is located within chromosome band 17q25.3 outside and telomeric of a region commonly deleted in breast and ovarian tumours. Cytogenetics and cell genetics 20 10894930
2011 Rac1 and Rac3 GTPases regulate the development of hilar mossy cells by affecting the migration of their precursors to the hilus. PloS one 19 21949760
2019 Rac3, but not Rac1, promotes ox-LDL induced endothelial dysfunction by downregulating autophagy. Journal of cellular physiology 18 31332791
2015 Silencing of Rac3 inhibits proliferation and induces apoptosis of human lung cancer cells. Asian Pacific journal of cancer prevention : APJCP 18 25854406
2006 Rac3-induced neuritogenesis requires binding to Neurabin I. Molecular biology of the cell 16 16525025
2021 Expression Analyses of Rac3, a Rho Family Small GTPase, during Mouse Brain Development. Developmental neuroscience 14 34839287
2015 RAC3 more than a nuclear receptor coactivator: a key inhibitor of senescence that is downregulated in aging. Cell death & disease 14 26469953
2005 Rac3-mediated transformation requires multiple effector pathways. Cancer research 13 16267012
2021 Rac3 Expression and its Clinicopathological Significance in Patients With Bladder Cancer. Pathology oncology research : POR 12 34257551
2014 The levels of RAC3 expression are up regulated by TNF in the inflammatory response. FEBS open bio 12 24918060
2012 Nuclear receptor coactivator RAC3 inhibits autophagy. Cancer science 12 22957814
2022 Hypomethylated gene RAC3 induces cell proliferation and invasion by increasing FASN expression in endometrial cancer. The international journal of biochemistry & cell biology 11 35917927
1998 Identification of a novel Rac3-interacting protein C1D. International journal of molecular medicine 11 9852280
2006 Nuclear localization of coactivator RAC3 is mediated by a bipartite NLS and importin alpha3. Biochemical and biophysical research communications 10 16875678
2024 Pulsatilla saponin D regulates ras-related C3 botulinum toxin substrate 3 (RAC3) to overcome resistance to paclitaxel in lung adenocarcinoma cells. BMC cancer 7 38200409
2024 An unusual presentation of de novo RAC3 variation in prenatal diagnosis. Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery 6 38214746
2021 Rac1 and Rac3 have opposite functions in Schwann cells during developmental myelination. Neuroscience letters 6 33812927
2018 Role of RAC3 coactivator in the adipocyte differentiation. Cell death discovery 6 30062065
2023 Rac1 and Rac3 GTPases and TPC2 are required for axonal outgrowth and migration of cortical interneurons. Journal of cell science 5 36744839
2021 Functional relationship between CFTR and RAC3 expression for maintaining cancer cell stemness in human colorectal cancer. Cellular oncology (Dordrecht, Netherlands) 5 33616840
2024 SETD8 inhibits apoptosis and ferroptosis of Ewing's sarcoma through YBX1/RAC3 axis. Cell death & disease 4 38987564
2024 Revealing the mechanisms of RAC3 in tumor aggressiveness, the immunotherapy response, and drug resistance in bladder cancer. Frontiers in oncology 4 39351351
2020 Upregulation of RAC3 in bladder cancer predicts adverse clinical outcome and increased tumor immune response. International journal of clinical and experimental pathology 4 33425095
2018 The inflammatory cytokine TNF contributes with RAC3-induced malignant transformation. EXCLI journal 4 30585274
2017 Study on the molecular mechanism of Rac3 on regulating autophagy in human lung cancer cells. Journal of B.U.ON. : official journal of the Balkan Union of Oncology 4 28534368
2024 Unveiling the role of RAC3 in the growth and invasion of cisplatin-resistant bladder cancer cells. Journal of cellular and molecular medicine 3 38847477
2024 The p.R66W Variant in RAC3 Causes Severe Fetopathy Through Variant-Specific Mechanisms. Cells 3 39682779
2007 [RAC3 nuclear receptor co-activator has a protective role in the apoptosis induced by different stimuli]. Medicina 3 18051230
2025 Prion-induced ferroptosis is facilitated by RAC3. Nature communications 2 40562790
2024 KLF1 Activates RAC3 to Mediate Fatty Acid Synthesis and Enhance Cisplatin Resistance in Bladder Cancer Cells. American journal of men's health 2 39376007
2011 [RAC3 overexpression is a transforming and proliferative signal that contributes to tumoral development]. Medicina 2 21296718
2011 Absence of Rac1 and Rac3 GTPases in the nervous system hinders thymic, splenic and immune-competence development. European journal of immunology 2 21469092
2025 A p.N92K variant of the GTPase RAC3 disrupts cortical neuron migration and axon elongation. The Journal of biological chemistry 1 40015633
2025 Prenatal diagnosis of a de novo 17q25.3 microdeletion encompassing RAC3 and CSNK1D in a fetus associated with partial agenesis of the corpus callosum, small brain volume, micrognathia and total anomalous pulmonary venous return. Taiwanese journal of obstetrics & gynecology 0 40049823
2025 A Pleiotropic and Functionally Divergent RAC3 Variant Disrupts Neurodevelopment and Impacts Organogenesis. Cells 0 41090727
2025 Rac3 promotes proliferation and invasion of endometrial cancer through the AKT/mTOR signalling pathway. Journal of obstetrics and gynaecology : the journal of the Institute of Obstetrics and Gynaecology 0 41123453
2025 Recurrent RAC3 related neuro-rachopathy in a pair of Indian siblings with novel findings: expanding the spectrum of brain anomalies. Clinical dysmorphology 0 41198064
2023 Dispensable role of Rac1 and Rac3 after cochlear hair cell specification. Journal of molecular medicine (Berlin, Germany) 0 37204479