Affinage

G3BP1

Ras GTPase-activating protein-binding protein 1 · UniProt Q13283

Length
466 aa
Mass
52.2 kDa
Annotated
2026-06-09
100 papers in source corpus 53 papers cited in narrative 53 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

G3BP1 is the central RNA-binding hub that nucleates stress granule (SG) assembly through RNA-dependent liquid-liquid phase separation (LLPS), and is essential for SG formation downstream of eIF2alpha phosphorylation or eIF4A inhibition (PMID:32302571, PMID:27022092). In unstressed cells it adopts a compact, auto-inhibited conformation stabilized by intramolecular electrostatic contacts between acidic intrinsically disordered tracts and the arginine-rich region; upon stress, mRNAs released from polysomes outcompete these contacts, triggering a conformational expansion that drives protein-RNA condensation (PMID:32302572). It functions as a condensate chaperone that promotes intermolecular RNA-RNA interactions to seed granules, after which it becomes dispensable for RNA condensate persistence, while DEAD-box helicase DDX3X resolves these interactions to keep condensates dynamic and translatable (PMID:39729994, PMID:39637853). G3BP1 condensation behavior is governed by mutually exclusive partners binding its NTF2-like domain — Caprin1 promoting and USP10 inhibiting assembly — and by 40S ribosome engagement through its RGG motif (PMID:27022092, PMID:37161291). A layered PTM code tunes its activity: CK2alpha phosphorylation at Ser149 disables RNA binding and disassembles granules (PMID:11604510, PMID:33065005), asymmetric arginine demethylation in the RGG domain promotes assembly (PMID:27601476), K376 acetylation by CBP/p300 (reversed by HDAC6) impairs RNA binding to facilitate disassembly (PMID:31481451), and ubiquitination controls granule turnover — K63-linked chains laid by TRIM21 inhibit LLPS while a FAF2/p97-VCP axis and autophagy receptors (p62, NDP52) clear ubiquitinated G3BP1 after stress (PMID:34739333, PMID:36692217). Beyond SGs, G3BP1 is an endoribonuclease that cleaves at CA dinucleotides and an ATP-dependent 5'->3' helicase, and it controls mRNA fate by binding structured 3' UTRs, rG4 structures, and specific transcripts to regulate decay and translation (PMID:11604510, PMID:9889278, PMID:32017897, PMID:34614161). In innate immunity it recruits PKR and Caprin1 to activate eIF2alpha phosphorylation and NF-kB/JNK signaling (PMID:25784705, PMID:25520508), promotes cGAS pre-condensation and DNA binding to drive interferon production and the senescence-associated secretory phenotype (PMID:30510222, PMID:34779554, PMID:33020468), and acts with RIG-I as a viral RNA co-sensor (PMID:30804210). G3BP1-dependent condensation of viral RNAs restricts replication of flaviviruses and SARS-CoV-2, which counter it via viral proteins bearing FGDF or phi-x-F/ITFG motifs that engage the NTF2-like domain (PMID:38295168, PMID:38492217, PMID:25658430). TDP-43 stabilizes G3BP1 transcripts via its 3' UTR, linking G3BP1 levels to ALS/FTD pathology (PMID:34115105).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1999 High

    Establishing G3BP1's earliest assigned enzymatic identity, biochemical purification revealed it is an ATP- and Mg2+-dependent nucleic acid helicase, framing the protein as an active RNA/DNA-remodeling enzyme rather than a passive binder.

    Evidence Purification from HeLa nuclear extract and in vitro helicase assays on partial duplex substrates

    PMID:9889278

    Open questions at the time
    • Physiological substrates of the helicase activity not defined
    • Relationship of helicase activity to later SG functions unresolved
  2. 2001 High

    Two foundational studies defined G3BP as a phosphorylation-regulated endoribonuclease (CA-cleavage) whose Ser149 status controls subcellular localization and mRNA stability, and showed its RNA-binding domain drives S-phase entry — establishing a direct link between G3BP and mRNA fate control.

    Evidence In vitro endoribonuclease assays with S149A/S149E mutants, c-myc mRNA stability assays, and RNA-binding-domain deletion in fibroblasts

    PMID:11146228 PMID:11604510

    Open questions at the time
    • Catalytic residues of the endoribonuclease not mapped
    • Downstream targets mediating S-phase entry undefined
  3. 2007 High

    Defining G3BP1's key protein interfaces, work mapped Caprin-1 binding to the NTF2-like domain via an FGDF-like motif and revealed G3BP1/2 sequestration of p53, beginning the dissection of how partner binding routes G3BP1 between granule and tumor-suppressor pathways.

    Evidence Motif mutagenesis with GST pulldown/Co-IP and subcellular fractionation/ubiquitylation assays

    PMID:17210633 PMID:17297477

    Open questions at the time
    • Structural basis of NTF2 motif recognition not yet solved at this stage
    • Functional consequence of p53 cytoplasmic redistribution in vivo unclear
  4. 2012 Medium

    Genetic dissection showed G3BP1/G3BP2 act redundantly to nucleate SGs and that SG size functions as a threshold switch triggering PKR-mediated eIF2alpha phosphorylation, connecting granule assembly to translational control.

    Evidence siRNA double-knockdown, heterodimerization Co-IP, and SG-size quantification in eIF2alpha-kinase-knockout MEFs

    PMID:22833567 PMID:23279204

    Open questions at the time
    • Molecular basis of the size threshold not defined
    • G3BP1 vs G3BP2 individual contributions partially overlapping
  5. 2015 High

    Multiple studies established the NTF2-like domain as the regulatory hub: USP10 and viral FGDF motifs compete there to inhibit assembly, while the PXXP domain recruits PKR to couple SG formation to NF-kB/JNK innate signaling and antiviral defense.

    Evidence FGDF-motif mutagenesis with crystallographic modeling, domain-deletion Co-IP, and viral replication/reporter assays

    PMID:25520508 PMID:25658430 PMID:25784705 PMID:25847539

    Open questions at the time
    • Quantitative competition between Caprin1/USP10/viral motifs not resolved
    • Mechanism of PKR activation independent of dsRNA incompletely defined
  6. 2016 High

    Convergent work defined the partner logic and PTM logic of SG control — establishing mutually exclusive Caprin1/USP10 binding, RGG-mediated 40S engagement, and arginine methylation by PRMT1/PRMT5 as a reversible stress-sensitive switch for assembly.

    Evidence CRISPR-KO rescue with defined mutants, ribosome fractionation, methylation-specific antibodies, and PRMT knockdown

    PMID:27022092 PMID:27513819 PMID:27601476

    Open questions at the time
    • Stoichiometry of competing partner occupancy unknown
    • Enzymes coupling stress to rapid demethylation not identified
  7. 2018 High

    Studies expanded G3BP1 into a nucleic-acid sensing hub, showing it promotes cGAS DNA-complex formation for interferon production and co-senses viral dsRNA with RIG-I via its RGG domain.

    Evidence Reciprocal Co-IP, dsRNA pulldown with in vitro translated protein, KO-cell IFN assays, and an in vivo AGS mouse model

    PMID:30510222 PMID:30804210

    Open questions at the time
    • How a single RGG domain selects DNA-sensing vs RNA-sensing contexts unclear
    • Relationship of immune sensing to SG condensation not fully separated
  8. 2019 Medium

    PTM and partner mapping refined disassembly and immune control: K376 acetylation (HDAC6/CBP) impairs RNA binding to drive SG resolution, eIF4GI was identified as an essential SG-forming partner, and G3BP1 was shown to stabilize RIG-I via RNF125.

    Evidence Acetyl-mimic mutants with RNA-binding/SG assays, domain-mapping Co-IP, and ubiquitination/viral replication assays

    PMID:30603102 PMID:31481451 PMID:31827077

    Open questions at the time
    • Temporal coordination of acetylation with other disassembly PTMs unresolved
    • Direct vs indirect effects on RIG-I stability not fully separated
  9. 2020 High

    Landmark reconstitution studies resolved the core mechanism: G3BP1 is an RNA-dependent LLPS switch held in an auto-inhibited compact state by electrostatic intramolecular contacts that free mRNA outcompetes upon stress, with IDR phosphorylation and cooperative partners tuning the transition.

    Evidence In vitro LLPS reconstitution, FRET/NMR, RNA competition assays, and IDR/phospho-site mutagenesis in two simultaneous Cell papers

    PMID:32302571 PMID:32302572

    Open questions at the time
    • In vivo confirmation of the conformational switch under physiological RNA loads incomplete
    • Quantitative contribution of each IDR to the threshold not isolated
  10. 2020 Medium

    Parallel work broadened G3BP1's regulatory and physiological reach — defining its role in structure-mediated mRNA decay with UPF1, cGAS pre-condensation, beta-F1-ATPase translational control, SASP activation, axonal granule control, and germline heat sensitivity via MAGE-B2-controlled abundance.

    Evidence RNA-seq with structured-3'UTR manipulation, cGAS LLPS imaging, TriFC/polysome profiling, and in vivo KO mouse models

    PMID:20663914 PMID:30135423 PMID:32017897 PMID:32692974 PMID:33020468 PMID:34779554

    Open questions at the time
    • Biochemical basis of recruitment to structured RNA not resolved
    • How a single concentration-threshold protein is tuned across tissues unclear
  11. 2021 Medium

    Studies defined the disassembly and turnover machinery and disease coupling: ubiquitinated G3BP1 is engaged by FAF2/p97-VCP for SG disassembly after heat shock, rG4-binding stabilizes target mRNAs, and TDP-43 stabilizes G3BP1 transcripts — tying G3BP1 levels to ALS/FTD.

    Evidence Ubiquitination-site mutants with Co-IP, in vitro rG4 binding with pyridostatin displacement, and TDP-43 CLIP-seq with patient-neuron analysis

    PMID:34115105 PMID:34614161 PMID:34739333

    Open questions at the time
    • E3 ligase generating disassembly-linked ubiquitin not identified at this stage
    • Causal contribution of G3BP1 loss to neurodegeneration not established
  12. 2023 Medium

    The ubiquitin and acetylation circuitry was completed: TRIM21 K63-ubiquitination inhibits LLPS with autophagy receptors clearing SGs, DCAF7/USP10 removes K48 ubiquitin at K76 to stabilize G3BP1, and SIRT2 deacetylation of G3BP1 dismantles the cGAS complex to restrain interferon.

    Evidence E3-ligase screens, in vitro ubiquitination/LLPS and deacetylation assays with site mapping, and KO models

    PMID:36692217 PMID:37870259 PMID:38973296

    Open questions at the time
    • Integration of competing ubiquitin linkages on the same molecule unresolved
    • Cross-talk between acetylation and ubiquitination codes not mapped
  13. 2024 High

    Reconstitution work reframed G3BP1 as a transient condensate chaperone that seeds RNA-RNA interactions and then becomes dispensable, with DDX3X and decondensers controlling condensate dynamics, and demonstrated G3BP1-driven viral RNA condensation as a direct antiviral restriction countered by SARS-CoV-2 N protein.

    Evidence In vitro RNA condensate reconstitution with decondenser inactivation, DDX3X disease-mutant assays, and structure-guided N-protein mutagenesis with in vivo infection

    PMID:38295168 PMID:38492217 PMID:39637853 PMID:39729994

    Open questions at the time
    • How decondensers are spatially regulated within granules unclear
    • Generality of RNA-only persistence across stress types untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the many competing inputs — conformational autoinhibition, the combinatorial PTM code, mutually exclusive NTF2 partners, and condensate-resolving helicases — are integrated quantitatively to set the SG assembly/disassembly threshold in a given cell state remains unresolved.
  • No unified quantitative model linking PTMs, partner occupancy, and RNA load to phase behavior
  • In vivo dynamics of competing regulators across tissues unmeasured

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 6 GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3 GO:0140098 catalytic activity, acting on RNA 3 GO:0016787 hydrolase activity 2 GO:0140657 ATP-dependent activity 2
Localization
GO:0005829 cytosol 3 GO:0005634 nucleus 2 GO:0005739 mitochondrion 1
Pathway
R-HSA-168256 Immune System 5 R-HSA-8953854 Metabolism of RNA 4 R-HSA-8953897 Cellular responses to stimuli 4 R-HSA-1643685 Disease 3 R-HSA-392499 Metabolism of proteins 3
Partners
CAPRIN1CGASDDX3XEIF4GIFAF2PKRRIG-IUSP10
Complex memberships
DCAF7-USP10-G3BP1 complexG3BP1-Caprin1-PKR complexcGAS-G3BP1 complexstress granule

Evidence

Reading pass · 53 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2020 G3BP1 functions as a molecular switch that triggers RNA-dependent liquid-liquid phase separation (LLPS) to assemble stress granules. Three distinct intrinsically disordered regions (IDRs) regulate its intrinsic propensity for LLPS, and phosphorylation within these IDRs fine-tunes this regulation. Extrinsic G3BP1-binding factors (e.g., Caprin1 promotes, USP10 inhibits) modulate SG assembly through positive or negative cooperativity. In vitro LLPS reconstitution, phase separation assays, mutagenesis of IDRs and phosphorylation sites, RNA-binding experiments Cell High 32302571
2020 Under non-stress conditions, G3BP1 adopts a compact auto-inhibited state stabilized by electrostatic intramolecular interactions between intrinsically disordered acidic tracts and the positively charged arginine-rich region. Upon release of mRNAs from polysomes during stress, unfolded mRNAs outcompete G3BP auto-inhibitory interactions, inducing a conformational transition that facilitates G3BP clustering through protein-RNA interactions and drives RNA/protein condensate formation. FRET, NMR, in vitro RNA competition assays, mutagenesis, live-cell imaging Cell High 32302572
2016 G3BP1 and G3BP2 double knockout abolishes SG formation in response to eIF2α phosphorylation or eIF4A inhibition. Caprin1 binding to G3BP1 promotes SG formation whereas USP10 binding inhibits SG formation; these interactions are mutually exclusive at G3BP1. G3BP1 interacts with 40S ribosomal subunits through its RGG motif, required for SG-mediated condensation. Phosphomimetic G3BP1-S149E fails to rescue SG formation. CRISPR/KO cell lines, rescue with G3BP1 mutants (S149E, F33W), Co-IP, ribosome fractionation The Journal of cell biology High 27022092
2021 Stress granule disassembly after heat shock specifically requires ubiquitination of G3BP1. Ubiquitinated G3BP1 interacts with the ER-associated protein FAF2, which engages the ubiquitin-dependent segregase p97/VCP, targeting the stress granule interaction network for disassembly. Cultured human cells, ubiquitination assays, Co-IP of G3BP1 with FAF2 and p97/VCP, G3BP1 ubiquitination mutants Science High 34739333
2018 G3BP1 physically interacts with cGAS and promotes formation of large cGAS complexes that enhance cGAS DNA binding and cGAS-dependent interferon production. G3BP1 deficiency leads to inefficient DNA binding by cGAS. The small molecule EGCG disrupts G3BP1-cGAS complexes and inhibits DNA-triggered cGAS activation. Co-IP, G3BP1 knockdown/KO cells, IFN production assays, in vivo mouse model (AGS) Nature immunology High 30510222
2001 G3BP is a phosphorylation-dependent endoribonuclease that cleaves between cytosine and adenine (CA) via its C-terminal RRM-type RNA binding motif. Phosphorylation at serine 149 controls its subcellular localization: a S149A mutant remains exclusively cytoplasmic whereas a phosphomimetic S149E mutant translocates to the nucleus. G3BP is tightly associated with c-myc mRNA in mouse embryonic fibroblasts, and c-myc mRNA decay is delayed in RasGAP-deficient fibroblasts lacking properly phosphorylated G3BP. In vitro endoribonuclease assay, RNA binding/cleavage specificity mapping, site-directed mutagenesis (S149A and S149E), subcellular fractionation, mRNA stability assays Molecular and cellular biology High 11604510
1999 G3BP1 (HDH VIII) functions as a DNA and RNA helicase with ATP- and Mg2+-dependent activity. It prefers partially unwound 3'-tailed substrates, moves along the bound strand in the 5' to 3' direction, and can unwind partial RNA/DNA and RNA/RNA duplexes. The RGG-box-rich C-terminal domain is analogous to that of other DNA/RNA helicases. Biochemical purification from HeLa nuclear extract, in vitro helicase assay, microsequencing Nucleic acids research High 9889278
2016 G3BP1 arginine residues in its RGG domain are asymmetrically dimethylated by PRMT1 and symmetrically methylated by PRMT5. Increased arginine methylation represses SG assembly, while decreased methylation promotes it. Arsenite stress rapidly and reversibly decreases asymmetric arginine methylation on G3BP1, acting as a regulatory signal for SG formation. Methylation-specific antibodies, PRMT1/PRMT5 knockdown/overexpression, in vitro methylation assay, SG formation assays The Journal of biological chemistry High 27601476
2007 Caprin-1 interacts with G3BP-1 via a conserved F(M/I/L)Q(D/E)Sx(I/L)D motif in Caprin-1 that binds the NTF2-like domain of G3BP-1. Caprin-1 and G3BP-1 co-localize in cytoplasmic RNA granules. The carboxy-terminal RGG motifs of Caprin-1 selectively bind c-Myc and cyclin D2 mRNAs. Caprin-1-mediated induction of eIF2α phosphorylation requires its mRNA-binding ability. Mutagenesis of Caprin-1 motifs, GST pulldown, co-immunoprecipitation, confocal microscopy, eIF2α phosphorylation assays Molecular and cellular biology High 17210633
2015 G3BP1 directly interacts with inactive PKR through both the NTF2-like and PXXP domains of G3BP1. Caprin1 also directly interacts with PKR and is required for efficient PKR activation at stress granules and release of active PKR into the cytoplasm. The G3BP1-Caprin1-PKR complex represents a mode of PKR activation independent of dsRNA pattern recognition, and the PXXP domain of G3BP1 is essential for PKR recruitment to SGs, eIF2α phosphorylation, and antiviral activity. Direct binding assays, Co-IP, G3BP1 domain deletion mutants, PKR activation assay (eIF2α phosphorylation), viral infection assays mBio High 25784705
2015 Viral proteins (e.g., SFV nsP3) and the cellular protein USP10 inhibit SG assembly via FGDF motifs that bind the NTF2-like domain of G3BP1. Both phenylalanine residues and the glycine in the FGDF motif are essential for binding. A crystal structure model of G3BP1-NTF2 bound to an FGDF-containing peptide was generated, revealing the binding mode. Mutagenesis of FGDF motifs, pulldown, SG formation assays, crystallographic modeling PLoS pathogens High 25658430
2022 The NTF2-like domain of G3BP1 contains a conserved surface groove targeted by SARS-CoV-2 nucleocapsid (N) protein residues 1-25 via a φ-x-F motif. Crystal structure of G3BP1-NTF2 in complex with N1-25 peptide revealed surface complementarity. Mutation of key interaction residues disrupts the G3BP1-N interaction in vitro. X-ray crystallography, isothermal titration calorimetry, mutagenesis, pulldown assays Journal of molecular biology High 35240128
2019 Acetylation of G3BP1 at lysine-376 (K376) within the RRM RNA-binding domain impairs RNA binding and disrupts RNA-dependent interaction with PABP1 (but not RNA-independent interactions with Caprin-1 or USP10). K376 acetylation is regulated by HDAC6 (eraser) and CBP/p300 (writer). Acetylated G3BP1 is detected outside SGs and increases during SG resolution, suggesting it facilitates SG disassembly. Acetylation-mimicking (K376Q) and deacetylation-mimicking (K376R) mutants, RNA binding assays, Co-IP, SG formation/dissolution assays, HDAC6/CBP overexpression and knockdown Molecular and cellular biology High 31481451
2020 G3BP1 is required for mRNA decay of transcripts with highly structured 3' UTRs (structure-mediated RNA decay), functioning with UPF1. Depletion of G3BP1 increases steady-state levels of mRNAs with highly structured 3' UTRs and highly structured circular RNAs. RNA-seq, G3BP1 knockdown, 3' UTR structural manipulation, half-life assays Molecular cell Medium 32017897
2018 G3BP1 directly binds to multiple sequences of the FMDV IRES element via its C-terminal region and interacts directly with polypyrimidine tract-binding protein and eIF4B. G3BP1 reduces local flexibility of the IRES element and negatively regulates both cap-dependent and IRES-dependent translation. G3BP1 is cleaved by FMDV 3C protease at E284. RNA EMSA, in vitro translation assays, Co-IP, FMDV infection with G3BP1 mutants The FEBS journal Medium 28755480
2012 G3BP2 forms homo-multimers and hetero-multimers with G3BP1. Double knockdown of G3BP1 and G3BP2 significantly reduces SG formation, whereas single knockdown of either partially reduces it. Overexpression of G3BP2 alone can induce SGs without stress, similar to G3BP1. siRNA knockdown, Co-IP for heterodimerization, SG formation assays (arsenite, hypoxia, heat shock) Genes to cells Medium 23279204
2012 Assembly of large G3BP-induced stress granules (but not small granules) precedes and triggers eIF2α phosphorylation via PKR. Stress granule size acts as a threshold switch for PKR-mediated eIF2α phosphorylation and translational repression. G3BP overexpression, MEF cells with eIF2α kinase knockouts, PKR-specific inhibition, eIF2α phosphorylation assays, SG size quantification Molecular biology of the cell Medium 22833567
2010 G3BP1 directly interacts with the 3' UTR of beta-F1-ATPase mRNA via its RRM domain (confirmed by RNA-bridged trimolecular fluorescence complementation). G3BP1 interaction with beta-F1 mRNA inhibits its translation at the initiation level. This RNP complex localizes to the periphery of mitochondria. Affinity chromatography, Co-IP, RNA FISH, TriFC assay, polysome profiling, immunoelectron microscopy Journal of cell science Medium 20663914
2018 G3BP1 binds to RIG-I via its C-terminal RGG domain and directly binds viral dsRNA/poly(I:C) also via the RGG domain. G3BP1 overexpression enhances RIG-I-induced IFN-β production, and G3BP1 co-localizes with RIG-I and infecting VSV in cells. Co-IP, biotin-labeled dsRNA pulldown, in vitro translated G3BP1 binding assay, confocal microscopy, IFN-β reporter assay The Journal of biological chemistry Medium 30804210
2019 G3BP1 forms a complex with RNF125 and RIG-I; this interaction leads to auto-ubiquitination of RNF125 and thereby reduced RNF125-mediated degradation of RIG-I, promoting RIG-I expression and antiviral signaling. Co-IP of G3BP1-RNF125-RIG-I complex, ubiquitination assays, G3BP1 KO cells, viral replication assays Cell death & disease Medium 31827077
2014 G3BP1 recruits PKR to stress granules via its PXXP domain. The G3BP1-SG-PKR axis links SG formation to innate immune transcriptional responses through NF-κB and JNK. Truncated G3BP1 unable to form SGs lacks antiviral activity against enteroviruses. G3BP1 domain deletion mutants, SG formation assays, PKR Co-IP, NF-κB/JNK reporter assays, viral replication assays Journal of virology Medium 25520508
2015 G3BP1 depletion or its upstream regulator TDP-43 disturbs normal interactions between stress granules and processing bodies (PBs), reducing SG-PB docking and impairing preservation of polyadenylated mRNA. Reintroduction of G3BP1 alone rescues SG-PB interactions and mRNA preservation. G3BP1 siRNA, TDP-43 siRNA, live-cell imaging of SG-PB interactions, mRNA stability assays, G3BP1 rescue experiments The Journal of cell biology Medium 25847539
2018 In axons, G3BP1 forms stress granule-like structures that co-localize with stored axonal mRNAs and limit their translation. Upon axotomy, G3BP1 granules disassemble (associated with increased phospho-G3BP1), releasing mRNAs for local translation to support axon regeneration. Dominant-negative G3BP disrupts axonal SG-like structures, activates intra-axonal translation, increases axon growth, and accelerates nerve regeneration in vivo. Dominant-negative G3BP overexpression, G3BP1 co-localization with axonal mRNAs by FISH, phospho-G3BP1 immunostaining, nerve regeneration in rat in vivo model Nature communications Medium 30135423
2020 CK2α phosphorylates G3BP1 at Ser149 in axons after injury. Phosphomimetic G3BP1 shows markedly decreased RNA binding in neurons compared to wild-type and non-phosphorylatable G3BP1, releasing axonal mRNAs for translation. CK2α translation itself is regulated by local mTOR-dependent translation and axoplasmic Ca2+ levels. In vitro kinase assay, phosphomimetic/non-phosphorylatable G3BP1 mutants, RNA binding assay, dual FRAP reporter for axonal translation, CK2α mRNA depletion from axons Current biology Medium 33065005
2023 TRIM21 E3 ubiquitin ligase catalyzes K63-linked ubiquitination of G3BP1, which inhibits G3BP1 LLPS in vitro and promotes SG dissolution. Autophagy receptors SQSTM1/p62 and CALCOCO2/NDP52 directly interact with G3BP1 at SG periphery to mediate SG elimination via autophagy. E3 ligase screen, in vitro ubiquitination assay, LLPS assay with ubiquitinated G3BP1, Co-IP of G3BP1 with p62/NDP52, SG formation/elimination assays in KO cells Autophagy Medium 36692217
2023 SIRT2 deacetylates G3BP1 at K257, K276, and K376, leading to disassembly of the cGAS-G3BP1 complex, thereby inhibiting cGAS DNA binding, cGAS droplet formation, and type I IFN production. SIRT2 deficiency elevates IFN expression after HSV-1 infection. Co-IP of SIRT2-G3BP1, in vitro deacetylation assay, acetylation site mapping, cGAS-G3BP1 complex disruption assay, cGAS DNA binding and LLPS assays, SIRT2 KO mouse model EMBO reports Medium 37870259
2020 G3BP1 promotes pre-condensation of cGAS into a primary liquid-phase state in resting cells, enabling more efficient DNA-induced LLPS and rapid cGAS activation. RNA does not activate cGAS and upon DNA challenge, G3BP1 dissociates from cGAS, allowing full cGAS-DNA condensation. High-resolution microscopy, G3BP1 KO cells, cGAS LLPS assays, G3BP1 inhibition, DNA vs. RNA stimulation experiments EMBO reports Medium 34779554
2020 MAGE-B2 suppresses SG formation by reducing G3BP1 protein levels below the critical concentration for phase separation through translational inhibition of G3BP1. Knockout of the MAGE-B2 mouse ortholog or overexpression of G3BP1 confers hypersensitivity of the male germline to heat stress in vivo. MAGE-B2 KO mice, G3BP1 overexpression in vivo, polysome profiling (translational inhibition), SG formation assays, heat stress survival Molecular cell Medium 32692974
2010 MK-STYX (a pseudophosphatase) interacts with G3BP1 and inhibits G3BP1-induced SG formation. The catalytically active mutant of MK-STYX shows dramatically reduced G3BP1 binding and impaired ability to inhibit SG assembly, indicating the inactive phosphatase conformation is required for G3BP1 interaction. Mass spectrometry identification, Co-IP, G3BP1-induced SG formation assays with MK-STYX wild-type and active-site mutant The Biochemical journal Medium 20180778
2007 G3BP1 and G3BP2 bind to p53 in vitro and in vivo. G3BP1/2 expression leads to redistribution of p53 from the nucleus to the cytoplasm. G3BP2 (but not G3BP1) additionally associates with MDM2, stabilizes MDM2, and reduces MDM2-mediated p53 ubiquitylation and degradation. Proteomic pulldown, Co-IP in cells, subcellular fractionation, ubiquitylation assay, shRNA knockdown Oncogene Medium 17297477
2011 G3BP binds to BART mRNA and degrades it via its endoribonuclease activity. Intracellular CD24 interacts with G3BP in stress granules and inhibits G3BP's specific endoribonuclease activity toward BART mRNA, leading to increased BART expression and reduced cell invasion. Co-IP of CD24-G3BP complex, mRNA stability/RNase assays, CD24 knockdown, in vivo orthotopic xenograft model Cancer research Medium 21266361
2020 PRMT8 methylates G3BP1 (the dendritic RNA-binding protein) at arginine residues and suppresses Rac1-PAK1 signaling to control actin cytoskeleton dynamics for dendritic spine maturation. PRMT8 depletion leads to overabundance of filopodia and mis-localization of excitatory synapses. PRMT8 KD in neurons, co-IP of PRMT8-G3BP1, in vitro methylation assay, Rac1-PAK1 activity assay, spine morphology imaging Cell reports Medium 32521269
2019 eIF4GI is critical for canonical SG formation by directly interacting with G3BP via amino acids 182-203 of eIF4GI and the RNA-binding domain of G3BP. Picornavirus 2A or L proteases block SG formation by disrupting eIF4GI-G3BP1 interaction. Co-IP, domain deletion mapping, rescue of SG formation by eIF4GI, 2A/L protease cleavage assay Cell discovery Medium 30603102
2021 G3BP1 interacts with and inactivates GSK-3β (via Co-IP), suppressing GSK-3β-mediated β-catenin phosphorylation and degradation. Elevated G3BP1 stabilizes β-catenin by inhibiting its ubiquitin-proteasome degradation, promoting nuclear accumulation of β-catenin and cell proliferation. Co-IP of G3BP1-GSK-3β, β-catenin ubiquitination assay, pharmacological disruption of G3BP1-GSK-3β interaction, G3BP1 overexpression/knockdown Acta pharmacologica Sinica Low 33536604
2021 G3BP1 interacts with SPOP and functions as a competitive inhibitor of the Cul3-SPOP E3 ubiquitin ligase. Elevated G3BP1 disables Cul3-SPOP activity, promoting AR signaling. AR directly upregulates G3BP1 transcription in a feed-forward manner. Co-IP of G3BP1-SPOP, competitive inhibition assay, transcriptomic analysis of AR targets, AR ChIP at G3BP1 promoter Nature communications Medium 34795264
2020 G3BP1 coordinates lysophagy activity at lysosomes via a G3BP1/TSC2 complex. Dysfunction of the G3BP1/TSC2 complex accelerates lysosomal damage and ferroptosis via mTOR pathway dysregulation. Co-IP of G3BP1-TSC2, G3BP1 KD in nucleus pulposus cells, lysosomal damage assays, mTOR inhibition rescue, in vivo IDD model Cell proliferation Low 36450665
2023 G3BP1 stabilizes IRP2 protein by binding to and suppressing translation of FBXL5 mRNA (encoding the E3 ligase component that ubiquitinates IRP2). This G3BP1-FBXL5-IRP2 axis elevates cellular labile iron and mediates arsenite-induced ferroptotic cell death. G3BP1 KO cells, RIP for G3BP1-FBXL5 mRNA interaction, polysome profiling, IRP2 stability assays, ferroptosis assays, in vivo kidney injury model Journal of hazardous materials Medium 38118197
2021 TDP-43 stabilizes G3BP1 transcripts by directly binding a conserved cis regulatory element in the G3BP1 3' UTR. Nuclear TDP-43 depletion is sufficient to reduce G3BP1 protein levels in vitro and in vivo. In ALS/FTD patient neurons with TDP-43 cytoplasmic inclusions/nuclear depletion, G3BP1 transcripts are reduced. CLIP-seq (TDP-43 binding to G3BP1 3'UTR), mRNA stability assays, conditional TDP-43 KO in vivo, patient neuron analysis Brain Medium 34115105
2016 Immunopurified G3BP1 complex from mouse brain contains USP10, CtBP1, Caprin-1, G3BP2a, and PSF. This complex preferentially binds intron-retaining transcripts and 3' UTRs. G3BP1 depletion in mouse cerebellum decreases intron retention, including for Grm5 (metabotropic glutamate receptor 5) mRNA. Immunopurification of G3BP1 complex, CLIP-seq, G3BP1 KO mice with RNA-seq for intron retention Journal of neurochemistry Medium 27513819
2024 G3BP1 preferentially binds unfolded RNA and drives assembly of RNP granule-like condensates that establish RNA-RNA interactions. These RNA-RNA interactions limit mobility and translatability of sequestered mRNAs. The DEAD-box helicase DDX3X resolves these RNA-RNA interactions inside condensates, rendering them dynamic and enabling mRNA translation; disease-associated catalytically inactive DDX3X variants fail to resolve RNA-RNA interactions. In vitro condensate/LLPS reconstitution, RNA mobility assays, translation assays with condensate-sequestered mRNAs, DDX3X WT vs. disease mutants Molecular cell High 39729994
2024 G3BP1 promotes intermolecular RNA-RNA interactions that stabilize RNA condensates and is a 'condensate chaperone' for initial granule assembly. After initial condensation, G3BP1 is dispensable for the RNA component of granules to persist in vitro and in cells when RNA decondensers are inactivated, demonstrating that RNA condensates can persist without G3BP1 once formed. In vitro RNA condensation assays, G3BP1 depletion in cells, inactivation of RNA decondensers (DCP1a, XRN1), FRAP, RNA-only granule persistence assays Molecular cell High 39637853
2024 G3BP1-dependent condensation of viral RNAs (West Nile virus, Zika virus, SARS-CoV-2) antagonizes viral replication by condensing untranslating viral mRNPs. G3BP1-dependent RNA condensation disrupts viral replication organelles and viral RNA replication. G3BP1 does not generally alter innate immune pathway activation. Viruses counteract this by inhibiting G3BP1 RNA condensing activity, hijacking eIF4A decondensing activity, or maintaining efficient translation. G3BP1 KO cells, viral RNA condensation assays, viral replication organelle imaging, innate immune pathway reporter assays, eIF4A inhibition experiments Science advances Medium 38295168
2024 SARS-CoV-2 nucleocapsid (N) protein interacts with G3BP1/2 via the F17 residue in an ITFG motif. N-F17A mutation causes specific loss of G3BP1/2 interaction, fails to inhibit SG assembly, shows decreased viral replication in cells, and causes decreased pathology in vivo. Mechanistically, the G3BP1-N interaction promotes infection by limiting sequestration of viral genomic RNA into stress granules. Structure-guided mutagenesis, Co-IP, SG formation assays, viral replication in cells, in vivo mouse infection model Cell reports High 38492217
2023 Gadd45β promotes G3BP1-mediated SG formation by directly interacting with the RNA-binding domain of G3BP1, dissolving G3BP1's autoinhibitory electrostatic intramolecular interaction and inducing conformational expansion. The acidic loop 1 and RNA-binding properties of Gadd45β increase RNA-binding affinity of the G3BP1-Gadd45β complex, promoting SG assembly and RLR-mediated interferon signaling. Co-IP, FRET/structural analysis of G3BP1 conformation, RNA binding assays, Gadd45β KO mice, viral infection Cell reports Medium 37917584
2021 G3BP1 binds guanine quadruplex (rG4) structures in mRNAs directly via its C-terminal RGG domain (enhanced by RRM domain). Pyridostatin (rG4 ligand) displaces G3BP1 from mRNA 3' UTRs in cells. G3BP1 positively regulates mRNA stability through its rG4-binding activity (luciferase reporter assay). eCLIP-seq bioinformatics, in vitro rG4 binding assay, seCLIP-seq with pyridostatin treatment, luciferase reporter for mRNA stability Nucleic acids research Medium 34614161
2023 DCAF7 serves as a scaffold protein facilitating interaction between USP10 and G3BP1, leading to removal of K48-linked ubiquitin from Lys76 of G3BP1, preventing its proteasomal degradation and promoting SG-like structure formation and chemoresistance. Co-IP of DCAF7-USP10-G3BP1 complex, ubiquitination site mapping (K76), SG formation assays, G3BP1 knockdown rescue Advanced science Medium 38973296
2023 SERBP1 interacts with G3BP1 and recruits 26S proteasome subunits (PSMD10, PSMA3) to SGs. SERBP1 depletion reduces 20S proteasome activity at SGs, mislocalizes VCP/FAF2, and diminishes K63-linked polyubiquitination of G3BP1 during SG recovery, impairing SG clearance. Co-IP of SERBP1-G3BP1-proteasome complex, proteasome activity assay, ubiquitination assay, SERBP1 KD with SG clearance readout, in vivo heat stress in testes Research Low 37223481
2020 G3BP1 is required for activation of the senescence-associated secretory phenotype (SASP) by promoting association of cGAS with cytosolic chromatin fragments during senescence. Through cGAS, G3BP1 activates the NF-κB and STAT3 pathways to promote SASP expression. G3BP1 depletion or pharmacological inhibition impairs the cGAS pathway and prevents SASP expression without affecting senescence commitment itself. G3BP1 KD/inhibition, cGAS-chromatin fragment Co-IP, NF-κB/STAT3 pathway readouts, in vitro and in vivo tumor growth assays Nature communications Medium 33020468
2004 G3BP-1 and HuD proteins associate in an RNA-dependent manner in differentiated P19 neuronal cells. IMP-1 associates with both HuD and G3BP-1 in an RNA-dependent manner and binds directly to tau mRNA, placing G3BP-1 in a tau mRNA-containing RNP granule complex. GST-HuD fusion pulldown from P19 cell lysates, Co-IP, RNA-dependent complex analysis, tau mRNA binding assay Journal of neurochemistry Low 15086518
2011 TDP-43 regulates the levels of G3BP mRNA (a SG nucleating factor). Disease-associated mutation TDP-43(R361S) is a loss-of-function mutation with respect to SG formation and alters G3BP and TIA-1 levels, while TDP-43(D169G) does not impact this pathway. TDP-43 KD, mRNA level analysis, TDP-43 mutant overexpression, SG formation assays Human molecular genetics Low 21257637
2002 Heregulin β1 (HRG) stimulation induces G3BP ATPase activity, promotes its phosphorylation (increasing association with GTPase-activating protein), and causes G3BP translocation to the nucleus where it co-localizes with acetylated histone H3 (active transcription sites). These effects are blocked by the HER2 antibody Herceptin. ATPase assay, Co-IP (G3BP-GAP), subcellular fractionation/immunofluorescence, Herceptin inhibition Cancer research Low 11888885
2001 G3BP promotes S phase entry in serum-deprived fibroblasts. This function is dependent on the presence of the RNA-binding domain of G3BP. G3BP overexpression in fibroblasts, RNA-binding domain deletion mutant, cell cycle analysis (S phase entry) Cancer letters Low 11146228
2023 Crystal structure of G3BP1-NTF2 in complex with a Caprin-1-derived short linear motif (SLiM) was solved. Caprin-1 interacts with His-31 and His-62 of G3BP1-NTF2 at a third binding site distinct from those used by USP10. G3BP1-NTF2 is destabilized at acidic pH, an effect counterbalanced better by USP10 than Caprin-1, suggesting pH modulates competitive binding. SG condensates are acidified ~0.5 pH units relative to cytosol. X-ray crystallography, nano-DSF, biophysical binding assays, ratiometric pH fluorescence imaging in cells Open biology High 37161291

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2020 G3BP1 Is a Tunable Switch that Triggers Phase Separation to Assemble Stress Granules. Cell 1005 32302571
2020 RNA-Induced Conformational Switching and Clustering of G3BP Drive Stress Granule Assembly by Condensation. Cell 672 32302572
2016 G3BP-Caprin1-USP10 complexes mediate stress granule condensation and associate with 40S subunits. The Journal of cell biology 517 27022092
2018 A G3BP1-Interacting lncRNA Promotes Ferroptosis and Apoptosis in Cancer via Nuclear Sequestration of p53. Cancer research 415 29588351
2011 TAR DNA-binding protein 43 (TDP-43) regulates stress granule dynamics via differential regulation of G3BP and TIA-1. Human molecular genetics 337 21257637
2021 Ubiquitination of G3BP1 mediates stress granule disassembly in a context-specific manner. Science (New York, N.Y.) 265 34739333
2018 G3BP1 promotes DNA binding and activation of cGAS. Nature immunology 254 30510222
2012 Both G3BP1 and G3BP2 contribute to stress granule formation. Genes to cells : devoted to molecular & cellular mechanisms 254 23279204
2020 Structure-Mediated RNA Decay by UPF1 and G3BP1. Molecular cell 224 32017897
2007 Distinct structural features of caprin-1 mediate its interaction with G3BP-1 and its induction of phosphorylation of eukaryotic translation initiation factor 2alpha, entry to cytoplasmic stress granules, and selective interaction with a subset of mRNAs. Molecular and cellular biology 219 17210633
2012 Contrasting pathology of the stress granule proteins TIA-1 and G3BP in tauopathies. The Journal of neuroscience : the official journal of the Society for Neuroscience 199 22699908
2014 The stress granule protein G3BP1 recruits protein kinase R to promote multiple innate immune antiviral responses. Journal of virology 173 25520508
2001 RasGAP-associated endoribonuclease G3Bp: selective RNA degradation and phosphorylation-dependent localization. Molecular and cellular biology 168 11604510
2016 Arginine Demethylation of G3BP1 Promotes Stress Granule Assembly. The Journal of biological chemistry 167 27601476
2016 New World and Old World Alphaviruses Have Evolved to Exploit Different Components of Stress Granules, FXR and G3BP Proteins, for Assembly of Viral Replication Complexes. PLoS pathogens 157 27509095
2018 Axonal G3BP1 stress granule protein limits axonal mRNA translation and nerve regeneration. Nature communications 145 30135423
2004 The insulin-like growth factor mRNA binding-protein IMP-1 and the Ras-regulatory protein G3BP associate with tau mRNA and HuD protein in differentiated P19 neuronal cells. Journal of neurochemistry 133 15086518
2015 Viral and cellular proteins containing FGDF motifs bind G3BP to block stress granule formation. PLoS pathogens 129 25658430
2015 Stress granules regulate double-stranded RNA-dependent protein kinase activation through a complex containing G3BP1 and Caprin1. mBio 128 25784705
2004 Rasputin, more promiscuous than ever: a review of G3BP. The International journal of developmental biology 127 15602692
2019 The stress granule protein G3BP1 binds viral dsRNA and RIG-I to enhance interferon-β response. The Journal of biological chemistry 112 30804210
2012 Large G3BP-induced granules trigger eIF2α phosphorylation. Molecular biology of the cell 111 22833567
2015 G3BP1 promotes stress-induced RNA granule interactions to preserve polyadenylated mRNA. The Journal of cell biology 102 25847539
2023 Stress granule homeostasis is modulated by TRIM21-mediated ubiquitination of G3BP1 and autophagy-dependent elimination of stress granules. Autophagy 95 36692217
2019 Foot-and-Mouth Disease Virus Leader Protease Cleaves G3BP1 and G3BP2 and Inhibits Stress Granule Formation. Journal of virology 90 30404792
2019 G3BP1 inhibits RNA virus replication by positively regulating RIG-I-mediated cellular antiviral response. Cell death & disease 89 31827077
2018 G3BP1 promotes tumor progression and metastasis through IL-6/G3BP1/STAT3 signaling axis in renal cell carcinomas. Cell death & disease 88 29717134
2020 G3BP1 controls the senescence-associated secretome and its impact on cancer progression. Nature communications 77 33020468
2019 The Acetylation of Lysine-376 of G3BP1 Regulates RNA Binding and Stress Granule Dynamics. Molecular and cellular biology 77 31481451
2001 G3BP is overexpressed in human tumors and promotes S phase entry. Cancer letters 76 11146228
2007 Modulation of p53 and MDM2 activity by novel interaction with Ras-GAP binding proteins (G3BP). Oncogene 74 17297477
2014 eEF2 and Ras-GAP SH3 domain-binding protein (G3BP1) modulate stress granule assembly during HIV-1 infection. Nature communications 71 25229650
2011 Intracellular CD24 inhibits cell invasion by posttranscriptional regulation of BART through interaction with G3BP. Cancer research 71 21266361
2021 The stress granule protein G3BP1 promotes pre-condensation of cGAS to allow rapid responses to DNA. EMBO reports 67 34779554
2021 The multi-functional RNA-binding protein G3BP1 and its potential implication in neurodegenerative disease. Journal of neurochemistry 65 33349931
2019 Separate domains of G3BP promote efficient clustering of alphavirus replication complexes and recruitment of the translation initiation machinery. PLoS pathogens 64 31199850
2019 The interaction of YBX1 with G3BP1 promotes renal cell carcinoma cell metastasis via YBX1/G3BP1-SPP1- NF-κB signaling axis. Journal of experimental & clinical cancer research : CR 64 31481087
2010 Human G3BP1 interacts with beta-F1-ATPase mRNA and inhibits its translation. Journal of cell science 64 20663914
2002 Heregulin induces expression, ATPase activity, and nuclear localization of G3BP, a Ras signaling component, in human breast tumors. Cancer research 63 11888885
2020 Translational Repression of G3BP in Cancer and Germ Cells Suppresses Stress Granules and Enhances Stress Tolerance. Molecular cell 58 32692974
2021 Research Progress on the Structure and Function of G3BP. Frontiers in immunology 57 34526993
2024 Identification of small molecule inhibitors of G3BP-driven stress granule formation. The Journal of cell biology 56 38284934
2021 Huntington's disease mice and human brain tissue exhibit increased G3BP1 granules and TDP43 mislocalization. The Journal of clinical investigation 53 33945510
2019 SG formation relies on eIF4GI-G3BP interaction which is targeted by picornavirus stress antagonists. Cell discovery 52 30603102
2018 The roles and mechanisms of G3BP1 in tumour promotion. Journal of drug targeting 52 30207743
2012 GAP161 targets and downregulates G3BP to suppress cell growth and potentiate cisplaitin-mediated cytotoxicity to colon carcinoma HCT116 cells. Cancer science 52 22703643
2024 Interaction between host G3BP and viral nucleocapsid protein regulates SARS-CoV-2 replication and pathogenicity. Cell reports 51 38492217
1999 Human DNA helicase VIII: a DNA and RNA helicase corresponding to the G3BP protein, an element of the ras transduction pathway. Nucleic acids research 51 9889278
2021 TDP-43 stabilizes G3BP1 mRNA: relevance to amyotrophic lateral sclerosis/frontotemporal dementia. Brain : a journal of neurology 50 34115105
2020 G3BP1-linked mRNA partitioning supports selective protein synthesis in response to oxidative stress. Nucleic acids research 48 32406909
2020 A Ca2+-Dependent Switch Activates Axonal Casein Kinase 2α Translation and Drives G3BP1 Granule Disassembly for Axon Regeneration. Current biology : CB 47 33065005
2023 Phase-separated nucleocapsid protein of SARS-CoV-2 suppresses cGAS-DNA recognition by disrupting cGAS-G3BP1 complex. Signal transduction and targeted therapy 46 37100798
2020 G3BP1 interacts with YWHAZ to regulate chemoresistance and predict adjuvant chemotherapy benefit in gastric cancer. British journal of cancer 45 32989225
2011 Revisiting G3BP1 as a RasGAP binding protein: sensitization of tumor cells to chemotherapy by the RasGAP 317-326 sequence does not involve G3BP1. PloS one 45 22205990
2017 G3BP1 interacts directly with the FMDV IRES and negatively regulates translation. The FEBS journal 43 28755480
2021 G3BP1 binds to guanine quadruplexes in mRNAs to modulate their stabilities. Nucleic acids research 42 34614161
2020 The RNA-Binding Protein Rasputin/G3BP Enhances the Stability and Translation of Its Target mRNAs. Cell reports 42 32160542
2011 The N-terminal domain of G3BP enhances cell motility and invasion by posttranscriptional regulation of BART. Molecular cancer research : MCR 42 21665939
2024 G3BP1 promotes intermolecular RNA-RNA interactions during RNA condensation. Molecular cell 41 39637853
2022 SARS-CoV-2 Nucleocapsid Protein Targets a Conserved Surface Groove of the NTF2-like Domain of G3BP1. Journal of molecular biology 41 35240128
2020 The Protein Arginine Methyltransferase PRMT8 and Substrate G3BP1 Control Rac1-PAK1 Signaling and Actin Cytoskeleton for Dendritic Spine Maturation. Cell reports 40 32521269
2018 Foot-and-Mouth Disease Virus Counteracts on Internal Ribosome Entry Site Suppression by G3BP1 and Inhibits G3BP1-Mediated Stress Granule Assembly via Post-Translational Mechanisms. Frontiers in immunology 40 29887867
2010 The pseudophosphatase MK-STYX interacts with G3BP and decreases stress granule formation. The Biochemical journal 40 20180778
2022 The roles of G3BP1 in human diseases (review). Gene 39 35176431
2023 KIF14 promotes proliferation, lymphatic metastasis and chemoresistance through G3BP1/YBX1 mediated NF-κB pathway in cholangiocarcinoma. Oncogene 38 36922675
2022 G3BP1 coordinates lysophagy activity to protect against compression-induced cell ferroptosis during intervertebral disc degeneration. Cell proliferation 36 36450665
2024 G3BP1-dependent condensation of translationally inactive viral RNAs antagonizes infection. Science advances 34 38295168
2023 Pro-Viral and Anti-Viral Roles of the RNA-Binding Protein G3BP1. Viruses 34 36851663
2021 G3BP1 promotes human breast cancer cell proliferation through coordinating with GSK-3β and stabilizing β-catenin. Acta pharmacologica Sinica 32 33536604
2021 G3BP1 inhibits Cul3SPOP to amplify AR signaling and promote prostate cancer. Nature communications 32 34795264
2018 A GTPase-activating protein-binding protein (G3BP1)/antiviral protein relay conveys arteriosclerotic Wnt signals in aortic smooth muscle cells. The Journal of biological chemistry 31 29626090
2023 SIRT2 negatively regulates the cGAS-STING pathway by deacetylating G3BP1. EMBO reports 30 37870259
2023 G3BP1 and SLU7 Jointly Promote Immune Evasion by Downregulating MHC-I via PI3K/Akt Activation in Bladder Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 30 38084438
2020 Seneca Valley Virus 3C Protease Inhibits Stress Granule Formation by Disrupting eIF4GI-G3BP1 Interaction. Frontiers in immunology 29 33133097
2011 Analysis of subcellular G3BP redistribution during rubella virus infection. The Journal of general virology 29 21994324
2023 The stress granule protein G3BP1 alleviates spinocerebellar ataxia-associated deficits. Brain : a journal of neurology 28 36511898
2019 GTPase-activating protein-binding protein 1 (G3BP1) plays an antiviral role against porcine epidemic diarrhea virus. Veterinary microbiology 28 31500725
2019 G3BP1 inhibits ubiquitinated protein aggregations induced by p62 and USP10. Scientific reports 28 31501480
2022 TDRD3 is an antiviral restriction factor that promotes IFN signaling with G3BP1. PLoS pathogens 26 35085371
2020 Sensitivity of Alphaviruses to G3BP Deletion Correlates with Efficiency of Replicase Polyprotein Processing. Journal of virology 26 31941782
2019 G3BP1 activates the TGF-β/Smad signaling pathway to promote gastric cancer. OncoTargets and therapy 26 31564899
2024 DCAF7 Acts as A Scaffold to Recruit USP10 for G3BP1 Deubiquitylation and Facilitates Chemoresistance and Metastasis in Nasopharyngeal Carcinoma. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 25 38973296
2021 Genomics-guided targeting of stress granule proteins G3BP1/2 to inhibit SARS-CoV-2 propagation. International journal of biological macromolecules 25 34517025
2023 G3BP1-dependent mechanism suppressing protein aggregation in Huntington's models and its demise upon stress granule assembly. Human molecular genetics 24 36611004
2015 G3BP1 restricts HIV-1 replication in macrophages and T-cells by sequestering viral RNA. Virology 24 26432022
2023 Caprin-1 binding to the critical stress granule protein G3BP1 is influenced by pH. Open biology 23 37161291
2019 G3BP1 Depletion Increases Radiosensitisation by Inducing Oxidative Stress in Response to DNA Damage. Anticancer research 23 31704836
2024 G3BP-driven RNP granules promote inhibitory RNA-RNA interactions resolved by DDX3X to regulate mRNA translatability. Molecular cell 22 39729994
2022 Upregulated LINC01088 facilitates malignant phenotypes and immune escape of colorectal cancer by regulating microRNAs/G3BP1/PD-L1 axis. Journal of cancer research and clinical oncology 22 35357586
2019 G3BP1 and G3BP2 regulate translation of interferon-stimulated genes: IFITM1, IFITM2 and IFITM3 in the cancer cell line MCF7. Molecular and cellular biochemistry 22 31172368
2001 Identification of metastasis associated gene G3BP by differential display in human cancer cell sublines with different metastatic potentials G3BP as highly expressed in non-metastatic. Chinese medical journal 22 11779432
2023 SERBP1 Promotes Stress Granule Clearance by Regulating 26S Proteasome Activity and G3BP1 Ubiquitination and Protects Male Germ Cells from Thermostimuli Damage. Research (Washington, D.C.) 21 37223481
2020 Overexpression of G3BP1 facilitates the progression of colon cancer by activating β‑catenin signaling. Molecular medicine reports 21 33000280
2019 G3BP1 knockdown sensitizes U87 glioblastoma cell line to Bortezomib by inhibiting stress granules assembly and potentializing apoptosis. Journal of neuro-oncology 21 31392596
2023 A regulatory module comprising G3BP1-FBXL5-IRP2 axis determines sodium arsenite-induced ferroptosis. Journal of hazardous materials 20 38118197
2022 CircEIF3H-IGF2BP2-HuR scaffold complex promotes TNBC progression via stabilizing HSPD1/RBM8A/G3BP1 mRNA. Cell death discovery 20 35568705
2016 Preferential binding of a stable G3BP ribonucleoprotein complex to intron-retaining transcripts in mouse brain and modulation of their expression in the cerebellum. Journal of neurochemistry 20 27513819
2021 G3BP1 Inhibition Alleviates Intracellular Nucleic Acid-Induced Autoimmune Responses. Journal of immunology (Baltimore, Md. : 1950) 19 33941659
1999 Upregulation of the RAS-GTPase activating protein (GAP)-binding protein (G3BP) in proliferating RPE cells. Journal of cellular biochemistry 19 10404389
2023 Gadd45β is critical for regulation of type I interferon signaling by facilitating G3BP-mediated stress granule formation. Cell reports 18 37917584

Missed literature

Know a paper Affinage missed for G3BP1? Flag it for the maintainers and the community.

No submissions yet.