Affinage

YWHAG

14-3-3 protein gamma · UniProt P61981

Length
247 aa
Mass
28.3 kDa
Annotated
2026-04-28
100 papers in source corpus 48 papers cited in narrative 48 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

YWHAG (14-3-3γ) is a phosphoserine/phosphothreonine-binding scaffold protein that functions as a homodimer to regulate cell cycle progression, apoptosis, membrane trafficking, and cytoskeletal dynamics across diverse cell types. In cell cycle control, 14-3-3γ binds Chk1 phosphorylated at Ser296 to mediate Cdc25A degradation and prevent premature mitotic entry after DNA damage (PMID:20639859), activates Plk1 via phospho-Ser99 binding to promote the metaphase-to-anaphase transition (PMID:23695676), constrains centrosome duplication through NPM1/Thr199 regulation (PMID:27253419), and stabilizes p53 by sequestering Chk1-phosphorylated MDMX (Ser367) in the cytoplasm while independently protecting p21 from MDMX-mediated degradation (PMID:16511572, PMID:21148311). As a membrane-trafficking scaffold, 14-3-3γ promotes plasma membrane delivery of ion channels (ANO1/Thr9, TRPM4b/Ser88, Best1/Ser358) and plakoglobin for desmosome assembly, and bridges CtBP1-S/BARS to PI4KIIIβ at the Golgi to drive carrier fission (PMID:22366688, PMID:27212225, PMID:25047048, PMID:24610948). Heterozygous missense mutations in the 14-3-3γ ligand-binding groove, particularly Arg132Cys, cause epileptic encephalopathy (PMID:33767733).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1999 Medium

    Establishing that 14-3-3γ is a substrate of multiple PKC isoforms and associates with Raf-1 linked PKC to MAPK signaling through this scaffold.

    Evidence Co-immunoprecipitation of 14-3-3γ with PKC isoforms and Raf-1 in PDGF-stimulated vascular smooth muscle cells

    PMID:10433554

    Open questions at the time
    • Phosphorylation sites on 14-3-3γ by PKC not mapped
    • Functional consequence of PKC-mediated phosphorylation on client binding not tested
  2. 2005 High

    Demonstrating that 14-3-3γ directly sequesters phospho-Bad to prevent mitochondrial apoptosis established a cytoprotective role for this isoform under stress, and that 14-3-3γ scaffolds AICD-FE65 complexes for gene transactivation linked it to APP signaling.

    Evidence Co-IP of 14-3-3γ with phospho-Bad in ischemic astrocytes with overexpression/knockdown survival assays; Co-IP of 14-3-3γ with AICD/FE65 and luciferase reporter transactivation assay

    PMID:15660102 PMID:16223726

    Open questions at the time
    • Whether Bad sequestration is isoform-specific among 14-3-3 family members
    • In vivo relevance of AICD-FE65 transactivation via 14-3-3γ not tested
  3. 2006 High

    Identifying Chk1-phosphorylated MDMX-Ser367 as a 14-3-3γ client revealed how DNA damage signals converge on p53 stabilization through cytoplasmic retention of MDMX, establishing a key checkpoint mechanism.

    Evidence MS-based affinity purification, Co-IP, K50E binding-defective mutant, siRNA, and kinase-dead Chk1 in UV-irradiated cells

    PMID:16511572

    Open questions at the time
    • Whether other 14-3-3 isoforms contribute to MDMX sequestration in parallel
    • Structural basis of K50E disruption not resolved
  4. 2006 High

    Showing phospho-GFAP (Ser8) binding to 14-3-3γ during G2/M with resulting intermediate filament disruption established a role in cytoskeletal remodeling during cell division.

    Evidence Co-IP, S→A mutagenesis of GFAP, cell-cycle synchronization, fluorescence imaging in astrocytes

    PMID:17032734

    Open questions at the time
    • Whether this regulates GFAP dynamics in vivo during astrocyte division
    • Other intermediate filament clients not explored
  5. 2010 High

    Demonstrating that 14-3-3γ binds Chk1-pSer296 to drive Cdc25A degradation after UV damage resolved the mechanism by which autophosphorylated Chk1 enforces the G2/M checkpoint, distinct from ATR-site phosphorylation.

    Evidence Co-IP, S296A mutant replacement of endogenous Chk1, cell cycle analysis after UV irradiation

    PMID:20639859

    Open questions at the time
    • Whether Chk1-pSer296/14-3-3γ complex has additional substrates beyond Cdc25A
    • Structural details of the ternary complex unknown
  6. 2010 High

    Showing that 14-3-3γ competitively displaces p21 from MDMX to stabilize p21 protein levels in p53-null cells established a p53-independent tumor-suppressive axis through cell cycle arrest.

    Evidence In vitro competition with purified proteins, pulse-chase half-life, G1 arrest in p53-null cells

    PMID:21148311

    Open questions at the time
    • Whether this competitive mechanism operates under physiological 14-3-3γ concentrations in vivo
    • MDMX binding site overlap with 14-3-3γ not structurally resolved
  7. 2012 High

    Reconstituting a 14-3-3γ dimer as a bridge between CtBP1-S/BARS and PI4KIIIβ at the Golgi, with carrier fission as the functional readout, established a direct scaffolding role in membrane trafficking.

    Evidence Complex reconstitution, reciprocal Co-IP, phosphorylation mutants, live-cell imaging of post-Golgi carriers

    PMID:22366688

    Open questions at the time
    • Whether 14-3-3γ acts catalytically or stoichiometrically in carrier fission
    • Lipid requirements for complex assembly not defined
  8. 2012 High

    Identifying 14-3-3γ binding to phospho-Ser194 of STAR at mitochondria, with time-dependent release enabling steroidogenesis, revealed a kinetic gating mechanism for hormone production.

    Evidence MS of native mitochondrial complexes, Co-IP, siRNA silencing with steroidogenesis readout

    PMID:22427666 PMID:25086053

    Open questions at the time
    • Whether Ser58 phosphorylation and Lys49 acetylation are mediated by specific kinases/acetyltransferases in vivo
    • Structural basis for STAR unfolding by 14-3-3γ unknown
  9. 2013 High

    Demonstrating that PI3K-Akt-phosphorylated Plk1 (Ser99) requires 14-3-3γ for catalytic activation connected growth factor signaling to mitotic progression and identified a new checkpoint control point.

    Evidence Co-IP, in vitro kinase assay, S99A mutant, PI3K/Akt inhibitors, mitotic arrest quantification

    PMID:23695676

    Open questions at the time
    • Whether 14-3-3γ activates Plk1 allosterically or by blocking an inhibitory interaction
    • Contribution of other 14-3-3 isoforms to Plk1 regulation
  10. 2014 High

    Establishing that 14-3-3γ promotes surface delivery of TRPM4b (via Ser88) and plakoglobin (via PKCμ phosphorylation and KIF5B motor) expanded the trafficking scaffold concept to ion channels and desmosomes, with rescue experiments confirming transport as the primary function.

    Evidence Y2H, GST pulldown, Co-IP, electrophysiology, surface biotinylation for TRPM4b; PKCμ inhibition, KIF5B KD, knockout rescue for plakoglobin

    PMID:24610948 PMID:25047048 PMID:29253567

    Open questions at the time
    • Mechanism by which 14-3-3γ couples to the KIF5B-KLC1 motor
    • Whether 14-3-3γ chaperones channel folding in addition to trafficking
  11. 2015 High

    In utero knockdown causing delayed radial migration of cortical neurons directly demonstrated a developmental neurobiology role, distinct from its cancer and checkpoint functions.

    Evidence In utero electroporation knockdown with time-lapse live imaging of brain slices

    PMID:26297819

    Open questions at the time
    • Client proteins mediating the migration phenotype not identified
    • Whether migration defect contributes to epilepsy phenotype in YWHAG mutation carriers
  12. 2016 High

    Showing that 14-3-3γ loss causes centrosome amplification via NPM1-Thr199 hyperphosphorylation linked its tumor-suppressive checkpoint role to centrosome biology and aneuploidy.

    Evidence 14-3-3γ KO with centrosome immunofluorescence, NPM1 phospho-analysis, cdc25C rescue mutant, in vivo tumor formation

    PMID:27253419

    Open questions at the time
    • Kinase responsible for NPM1-Thr199 hyperphosphorylation when 14-3-3γ is lost
    • Whether centrosome defects underlie neuronal phenotypes
  13. 2017 High

    Identifying PAK6 phosphorylation of 14-3-3γ at Ser59 as a global client-release switch that rescues LRRK2-G2019S neurite shortening revealed a mechanism for upstream regulation of 14-3-3γ scaffold function in neurodegeneration.

    Evidence In vitro kinase assay, Co-IP, constitutively active PAK6 rescue of LRRK2-G2019S neuronal morphology

    PMID:29311810

    Open questions at the time
    • Whether Ser59 phosphorylation dissociates all clients or a subset
    • In vivo relevance in Parkinson's disease models not tested
  14. 2019 Medium

    Demonstrating isoform-specific regulation of Beclin-1-dependent autophagy — where starvation shifts 14-3-3γ from Beclin-1 to phospho-β-catenin — established a unique autophagy-activating role not shared by other 14-3-3 family members.

    Evidence Co-IP of 14-3-3γ with Beclin-1 and p-β-catenin, isoform-specific KO, autophagy flux assay in neurons

    PMID:30635843

    Open questions at the time
    • Kinase phosphorylating β-catenin to create the competing 14-3-3γ binding site not identified
    • Whether this autophagy mechanism operates in non-neuronal cells
  15. 2021 Medium

    Identification of de novo YWHAG missense mutations in epileptic encephalopathy patients, clustering in the ligand-binding groove, established YWHAG as a disease gene, connecting its scaffolding function to brain development.

    Evidence Trio-based whole exome sequencing, structural mapping of mutations to binding groove and dimerization domains, genotype-phenotype correlation

    PMID:33767733

    Open questions at the time
    • No in vitro functional validation of individual mutations
    • Whether haploinsufficiency or dominant-negative mechanism predominates
    • Animal model of disease-associated mutations not reported
  16. 2023 Medium

    Linking 14-3-3γ to cytoprotection during EMT via autophagy-mediated ROS suppression integrated its autophagy and pro-survival functions into a metastasis-enabling mechanism.

    Evidence YWHAG KD with ROS accumulation and autophagy flux measurement, kinome/transcriptome profiling, tumor allograft survival

    PMID:37759388

    Open questions at the time
    • Direct autophagy substrates downstream of 14-3-3γ during EMT not identified
    • Whether Beclin-1 pathway mediates this or an alternative autophagy route

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis by which Ser59 phosphorylation globally disrupts client binding, whether checkpoint versus trafficking functions are regulated independently in vivo, and the mechanistic link between binding-groove mutations and epileptic encephalopathy pathophysiology.
  • No high-resolution structure of 14-3-3γ with a full-length client
  • Isoform-specific versus redundant functions among 14-3-3 family members not systematically resolved
  • No mouse model recapitulating YWHAG epileptic encephalopathy mutations

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 11 GO:0098772 molecular function regulator activity 4
Localization
GO:0005886 plasma membrane 4 GO:0005829 cytosol 3 GO:0005739 mitochondrion 2 GO:0005794 Golgi apparatus 2 GO:0005634 nucleus 1 GO:0005815 microtubule organizing center 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 6 R-HSA-162582 Signal Transduction 5 R-HSA-1640170 Cell Cycle 5 R-HSA-1500931 Cell-Cell communication 2 R-HSA-5357801 Programmed Cell Death 2 R-HSA-73894 DNA Repair 2 R-HSA-9612973 Autophagy 2 R-HSA-1266738 Developmental Biology 1 R-HSA-168256 Immune System 1
Partners
BADCHEK1CTBP1LRRK2MDMXPI4KBPLK1STAR
Complex memberships
Chk1-pSer296–14-3-3γ checkpoint complexCtBP1-S/BARS–14-3-3γ–PI4KIIIβ Golgi fission complex

Evidence

Reading pass · 48 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 14-3-3γ binds to MDMX phosphorylated at Ser367 by Chk1 in response to UV irradiation, causing cytoplasmic retention of MDMX and suppression of MDMX-enhanced p53 ubiquitination, leading to p53 stabilization and activation. The 14-3-3γ mutant K50E that cannot bind MDMX lost this activity. Immuno-affinity purification/mass spectrometry, in vitro binding assay, co-immunoprecipitation, siRNA knockdown, kinase-dead Chk1 mutant, kinase inhibitor (UCN-01) The EMBO journal High 16511572
2010 14-3-3γ forms a complex with Chk1 phosphorylated at Ser296 (autophosphorylation site) but not at ATR sites (Ser317/345), and this ternary complex mediates phosphorylation and degradation of Cdc25A to block premature mitotic entry after DNA damage. Replacement of endogenous Chk1 with S296A mutant induced premature mitotic entry after UV irradiation. Co-immunoprecipitation, phospho-specific antibodies, UV irradiation, Chk1 S296A mutant replacement, siRNA knockdown, cell cycle analysis The EMBO journal High 20639859
2013 PI3K-Akt-dependent phosphorylation of Plk1 at Ser99 creates a docking site for 14-3-3γ; this interaction stimulates Plk1 catalytic activity. Knockdown of 14-3-3γ or the Plk1-S99A phospho-blocking mutant causes prometaphase/metaphase arrest via spindle assembly checkpoint activation, impairing metaphase-to-anaphase transition. Co-immunoprecipitation, kinase activity assay, siRNA knockdown, phospho-blocking mutant (S99A), PI3K/Akt inhibitors, mitotic cell cycle analysis Nature communications High 23695676
2012 14-3-3γ dimers serve as a scaffold bridging CtBP1-S/BARS to PI(4)KIIIβ at the Golgi; the complex is stabilized by PKD and PAK phosphorylation. Disrupting this association inhibits fission of elongating post-Golgi carrier precursors. Co-immunoprecipitation, protein complex reconstitution, dominant-negative and phosphorylation mutants, live-cell imaging of carrier formation Nature cell biology High 22366688
2017 PAK6 phosphorylates 14-3-3γ at Ser59, and this phosphorylation acts as a switch that dissociates 14-3-3γ from client proteins including LRRK2 at phospho-Ser935, causing LRRK2 dephosphorylation. Constitutively active PAK6 rescues G2019S LRRK2-associated neurite shortening through 14-3-3γ phosphorylation. Co-immunoprecipitation, in vitro kinase assay, phospho-specific antibodies, constitutively active PAK6 overexpression, neuronal morphology assay Frontiers in molecular neuroscience High 29311810
2012 14-3-3γ negatively regulates steroidogenesis by binding to Ser194 of STAR (the phosphorylation site in the START domain induced by hCG/cAMP), keeping STAR in an unfolded state. Over time, 14-3-3γ homodimerizes and dissociates from STAR, allowing maximal steroidogenesis. 14-3-3γ was identified in native mitochondrial complexes by mass spectrometry. Mass spectrometry of native mitochondrial complexes, immunoprecipitation, siRNA silencing, site-specific binding motif identification (Ser194) The Journal of biological chemistry High 22427666
2014 Ser58 phosphorylation and Lys49 acetylation of 14-3-3γ regulate its homodimerization and STAR binding in a coordinated time-dependent manner during cAMP-induced steroidogenesis. Blocking Ser58 phosphorylation or Lys49 acetylation with TAT-coupled peptides further induced steroidogenesis while reducing lipid storage. TAT-coupled phospho/acetylation blocking peptides, mass spectrometry, immunoprecipitation, steroidogenesis functional assay The Journal of biological chemistry High 25086053
2014 Phosphorylated tyrosine hydroxylase (TH) at Ser19 binds 14-3-3γ with high affinity (Kd = 3.2 nM); one TH tetramer binds one or two 14-3-3γ dimers. 14-3-3γ inhibits PKA-mediated phosphorylation of TH at Ser40 (~3.5-fold), and Ser40 phosphorylation does not significantly contribute to 14-3-3γ binding. Native mass spectrometry, surface plasmon resonance, electron microscopy, phosphatase kinetic assay, in vitro kinase assay Molecular & cellular proteomics High 24947669
2006 14-3-3γ associates with phosphorylated GFAP in a phosphorylation- and cell-cycle-dependent manner in astrocytes, with increased association during G2/M due to greater GFAP phosphorylation. Serine 8 in the GFAP head domain is essential for direct association with 14-3-3γ. Overexpression of 14-3-3γ disrupts GFAP intermediate filament integrity and dynamics. Co-immunoprecipitation, domain deletion and S→A substitution mutants of GFAP, cell-cycle synchronization, fluorescence imaging of intermediate filaments Journal of cell science High 17032734
2005 In ischemic astrocytes, 14-3-3γ is selectively induced and binds phospho-Bad, preventing Bad from translocating to mitochondria and thereby inhibiting apoptosis. Overexpression of 14-3-3γ promotes astrocyte survival while antisense knockdown enhances apoptosis under ischemia. Co-immunoprecipitation of endogenous 14-3-3γ with p-Bad, overexpression and antisense knockdown, apoptosis assays, ischemia model Journal of cerebral blood flow and metabolism High 15660102
2014 14-3-3γ is required for transport of plakoglobin to cell borders, and this transport depends on PKCμ-mediated phosphorylation of plakoglobin and the KIF5B-KLC1 microtubule motor complex. Loss of 14-3-3γ reduces desmosome assembly and cell-cell adhesion in vitro and in mouse testis in vivo. Co-immunoprecipitation, PKCμ inhibition, KIF5B knockdown, cell surface imaging, testis histology in knockout mice Journal of cell science High 24610948
2016 14-3-3γ promotes surface expression of ANO1 (Ca2+-activated Cl- channel) by binding to Thr9 in its N-terminus; gene silencing of 14-3-3γ reduces ANO1 surface expression and inhibits migration and invasion of glioblastoma cells. Yeast two-hybrid screening, co-immunoprecipitation, T9A mutagenesis, gene silencing, surface biotinylation, migration/invasion assays Scientific reports High 27212225
2014 14-3-3γ promotes surface expression of TRPM4b channels by binding to Ser88 at the TRPM4b N-terminus. Overexpression of 14-3-3γ increases TRPM4b plasma membrane expression and whole-cell currents; 14-3-3γ shRNA reduces surface expression, attenuates glutamate-induced TRPM4b currents, and protects hippocampal neurons from glutamate-induced cell death. Yeast two-hybrid, GST pull-down, co-immunoprecipitation, whole-cell patch clamp, cell surface biotinylation, shRNA knockdown, neuronal cell death assay Molecular brain High 25047048
2017 14-3-3γ promotes surface expression of Best1 (bestrophin-1) calcium-activated anion channel in astrocytes through direct interaction dependent on phosphorylation of Ser358 in the Best1 C-terminus. 14-3-3γ knockdown reduces Best1-mediated whole-cell current and glutamate release from hippocampal astrocytes. Yeast two-hybrid, BiFC interaction assay, whole-cell patch clamp, structural modeling, shRNA knockdown, CA1 pyramidal neuron current recording in hippocampal slices Molecular brain High 29121962
2016 14-3-3γ loss leads to centrosome amplification via phosphorylation of NPM1 at Thr199, causing early centriole disjunction and centrosome hyper-duplication; 14-3-3γ normally localizes to the centrosome. Loss leads to aneuploidy and increased tumor formation in mice. Expression of cdc25C S216A (14-3-3-binding-defective) in knockdown cells increased multipolar spindles and decreased tumor growth. 14-3-3γ knockdown/knockout, centrosome immunofluorescence, NPM1 phospho-specific analysis, cdc25C mutant rescue, tumor formation assay in mice Scientific reports High 27253419
2015 14-3-3γ ablation in utero results in delayed radial migration of pyramidal neurons and morphological defects (thicker leading process, failure to reach cortical plate-marginal zone boundary) in the developing cerebral cortex, demonstrated by time-lapse live imaging of brain slices. In utero electroporation-mediated knockdown, time-lapse live imaging of cortical brain slices, morphological quantification Developmental neurobiology High 26297819
2010 14-3-3γ induces oncogenic transformation of NIH3T3 cells and activates both MAP kinase and PI3K signaling pathways. 14-3-3γ co-immunoprecipitates with PI3K and TSC2, suggesting it stimulates PI3K signaling at two pathway points. Focus formation assay, tumor formation in SCID mice, co-immunoprecipitation of PI3K and TSC2, MAPK/PI3K inhibitor treatment PloS one Medium 20628654
2005 14-3-3γ dimers bind both AICD (amyloid beta-protein precursor intracellular domain) and FE65 simultaneously via the 667VTPEER672 motif of AICD, facilitating FE65-dependent gene transactivation. Phosphorylation of AICD at Thr668 inhibits this interaction and blocks gene transactivation. Co-immunoprecipitation of endogenous and exogenous proteins, luciferase reporter gene transactivation assay, phospho-Thr668 blocking experiments, deletion mutant analysis The Journal of biological chemistry High 16223726
2003 14-3-3γ binds to c-Raf-1 and p-Raf259 (Raf kinase) in primary astrocytes as demonstrated by co-immunoprecipitation; expression is upregulated by ischemia but this induction is independent of PI-3 kinase and MAP kinase pathways. Co-immunoprecipitation of endogenous proteins, pharmacological pathway inhibition (U0126, LY294002), Northern/Western blot Glia Medium 12730952
2009 Ischemia-induced upregulation of 14-3-3γ in astrocytes is mediated by the JNK/p-c-Jun/AP-1 signaling pathway; only JNK inhibition (SP600125) or AP-1 inhibition (curcumin) suppressed 14-3-3γ upregulation, while PI3K, ERK, and p38 inhibitors had no effect. Pharmacological inhibitors (SP600125, U0126, LY294002, SB203580), AP-1 inhibition, immunostaining of nuclear p-c-Jun, Western blot for 14-3-3γ Journal of neurochemistry Medium 19393026
1999 14-3-3γ protein is phosphorylated by multiple PKC isoforms (alpha, beta, gamma, theta, delta) in PDGF-stimulated human vascular smooth muscle cells, and interacts with Raf-1, suggesting a link between PKC and Raf-1 signaling. Co-immunoprecipitation of 14-3-3γ with PKC isoforms and Raf-1, PKC inhibitor treatment, PKC activator treatment, phosphorylation assays DNA and cell biology Medium 10433554
2002 14-3-3γ co-immunoprecipitates with detergent-soluble actin in astrocytes; co-localization with F-actin increases after ischemia, and during apoptosis 14-3-3γ dissociates from actin filaments. During mitosis, 14-3-3γ forms a ring-like structure enclosing F-actin around daughter nuclei. Reciprocal co-immunoprecipitation, immunofluorescence co-localization, cell division and ischemia models Biochemical and biophysical research communications Medium 12176032
2006 Phosphorylated Hsp20 (but not unphosphorylated Hsp20 or S16D phosphomimetic mutant) forms a tight complex with 14-3-3γ dimer; a dimer of 14-3-3 binds a dimer of Hsp20. 14-3-3γ increases the chaperone activity of phosphorylated Hsp20 toward insulin as a substrate. Size-exclusion chromatography, chemical crosslinking, chaperone activity assay with model substrates Molecular and cellular biochemistry Medium 17109079
2012 14-3-3γ binds supercoiled DNA preferentially over linear DNA, with strong affinity for cruciform DNA structures. 14-3-3γ co-localizes with DNA cruciforms in HCT-116 cells. Electrophoretic mobility shift assay (EMSA) on agarose gels, competition assay with magnetic beads, confocal microscopy in HCT-116 cells Journal of biomolecular structure & dynamics Medium 22856523
2012 14-3-3γ peripheral membrane binding to phospholipid bilayers is stimulated when complexed with Ser19-phosphorylated tyrosine hydroxylase peptide; isoform-specific histidine residues His158 and His195 are pivotal for ligand-induced membrane interaction, as shown by site-directed mutagenesis. Surface plasmon resonance on phospholipid bilayers, site-directed mutagenesis (H158 and H195), molecular dynamics simulations, electrostatic analysis of crystal structures PloS one High 23189152
2012 14-3-3γ was identified as a Mieap-interacting protein during MALM (Mieap-induced accumulation of lysosome-like organelles within mitochondria); 14-3-3γ localizes within mitochondria during MALM and is required for elimination of oxidized mitochondrial proteins, but not for accumulation of Mieap or lysosomal proteins. 2DICAL mass spectrometry of immunoprecipitated Mieap complexes, co-immunoprecipitation of endogenous proteins, immunofluorescence localization, 14-3-3γ deficiency analysis Scientific reports Medium 22532927
2013 14-3-3γ targets AID to immunoglobulin switch regions (containing 5'-AGCT-3' repeats) to mediate class switch DNA recombination. 14-3-3γ expression in B cells is induced rapidly by CSR stimuli via NF-κB recruitment to the 14-3-3γ promoter, which enables CFP1/COMPASS-mediated H3K4me3 at the promoter, and is sustained by E2A binding to a downstream E-box. ChIP for NF-κB and CFP1 at 14-3-3γ promoter, H3K4me3 ChIP, luciferase reporter, B cell CSR assay, germinal center immunostaining Journal of immunology Medium 23851690
2010 14-3-3γ overexpression causes abnormal DNA replication and polyploidization in H322 lung cancer cells. Polyploid cells are resistant to microtubule inhibitors and can reenter the cell cycle in the absence of mitosis (endoreduplication), suggesting 14-3-3γ enables bypass of the mitotic checkpoint. Overexpression in H322 cells, flow cytometry, microtubule inhibitor treatment, cell cycle re-entry analysis Molecular carcinogenesis Medium 17394238
2012 14-3-3γ oncogenic transformation and activation of PI3K and MAPK signaling requires specific amino acids in the N-terminal variable region II (VRII, first 40 amino acids); swapping VRII between 14-3-3γ and tumor-suppressor 14-3-3σ transfers the respective oncogenic or suppressive phenotype. Chimeric protein domain swaps, individual amino acid substitutions, focus formation assay, soft agar growth, PI3K/MAPK pathway analysis The Journal of biological chemistry Medium 23115241
2010 14-3-3γ inhibits MDMX-mediated proteasomal degradation of p21 in a p53-independent manner: 14-3-3γ overexpression extends p21 half-life and causes G1 arrest in p53-null cells. 14-3-3γ competitively excludes p21 from binding MDMX in a dose-dependent fashion, as shown with purified proteins in vitro. In vitro competitive co-immunoprecipitation with purified proteins, pulse-chase half-life assay, p53-null cell lines, siRNA knockdown, cell cycle analysis The Journal of biological chemistry High 21148311
2012 Hypoxia activates ATR-Chk1 cascade to phosphorylate MDMX at Ser367, enhancing binding to 14-3-3γ and leading to p53 activation. ATR/Chk1 knockdown and Chk1 inhibitor impaired MDMX Ser367 phosphorylation and 14-3-3γ-MDMX binding; primary MEFs with MDMX S367A mutation failed to show 14-3-3γ binding or p53 activation under hypoxia. Co-immunoprecipitation, Chk1 inhibitor, ATR/Chk1 siRNA knockdown, MDMX S367A knock-in MEFs, hypoxia model The Journal of biological chemistry High 22556425
2015 CK2 (protein kinase CK2) interacts with 14-3-3γ at the neuromuscular junction and phosphorylates 14-3-3γ at serine residue 235. Co-immunoprecipitation, in vitro kinase assay, NMJ localization studies, phospho-site mapping The Journal of biological chemistry Medium 26198629
2014 14-3-3γ interacts with eIF1AX and RPS7 (ribosomal/translation initiation factors), as identified by co-immunoprecipitation coupled with MALDI-TOF/TOF mass spectrometry and confirmed by FRET; 14-3-3γ overexpression positively regulates mTOR pathway, Stat5 expression, and protein synthesis in bovine mammary epithelial cells. Co-immunoprecipitation with MALDI-TOF/TOF mass spectrometry, FRET, co-localization, overexpression and knockdown with protein synthesis readouts Archives of biochemistry and biophysics Medium 25281768
2015 A mitotic PI4KIIIβ-14-3-3γ complex mediates Golgi translocation of ERK1c; CDK1 phosphorylates ERK1c at Ser343, enabling binding to this complex, and PKD phosphorylation of PI4KIIIβ stabilizes the complex. At the Golgi, ERK1c is activated by MEK1b to induce Golgi fragmentation during mitosis. Co-immunoprecipitation, CDK1 and PKD phosphorylation mutants, live-cell imaging of Golgi fragmentation, dominant-negative constructs Journal of cell science Medium 26459638
2015 14-3-3γ loss leads to decreased desmosome function due to defective transport of plakoglobin to the cell border; artificially targeting plakoglobin (PG-EGFP-f) to the cell border in 14-3-3γ knockout cells restores desmosome formation, demonstrating that the primary role of 14-3-3γ in desmosome assembly is plakoglobin transport. 14-3-3γ knockout, PG-EGFP-f forced localization rescue, desmosome immunofluorescence, cell adhesion assay Biochemical and biophysical research communications Medium 29253567
2018 14-3-3γ binds RGS14 at two distinct sites: a phosphorylation-independent site that inhibits RGS14 nuclear import, and a phosphorylation-dependent site at Ser218 (potentiated by active H-Ras signaling) that inhibits active Gαi1-AlF4- binding to the RGS domain. These two binding modes selectively regulate distinct RGS14 functions. Bioluminescence resonance energy transfer (BRET), co-immunoprecipitation, phospho-blocking mutants, Ras signaling manipulation The Journal of biological chemistry High 30093406
2014 14-3-3γ overexpression in LPS-treated cardiomyocytes associates with phospho-Bad(S112) via co-immunoprecipitation, facilitates Bad disassociation from Bcl-2, and promotes Bcl-2 translocation to mitochondria, preventing mPTP opening and maintaining mitochondrial membrane potential. Co-immunoprecipitation, subcellular fractionation Western blot, flow cytometry (ΔΨm and apoptosis), mitochondrial swelling assay, overexpression with pFLAG International immunopharmacology Medium 24957688
2017 14-3-3γ directly interacts with Copine1 (CPNE1) through the C2A domain of CPNE1, with Ser54 being critical for this interaction; among all 14-3-3 isoforms, only 14-3-3γ binds CPNE1. Overexpression of 14-3-3γ in CPNE1-high HiB5 cells increases AKT phosphorylation, neurite outgrowth, and neuronal marker expression. Yeast two-hybrid, in vitro and in vivo co-immunoprecipitation, isoform specificity test, Ser54 mutagenesis, neurite outgrowth assay Experimental cell research Medium 28412242
2003 14-3-3γ is poly-ADP-ribosylated in the nucleus after traumatic brain injury, as identified by a proteomics approach; complete inhibition of poly-ADP-ribosylation at a dose that profoundly impairs spatial memory is associated with loss of 14-3-3γ ribosylation. Proteomics identification of poly-ADP-ribosylated peptides, PARP inhibitor dose-response (INH2BP), Morris water maze behavioral assay Journal of neurochemistry Medium 12694396
2021 YWHAG interacts with TMOD3 (tropomodulin 3), as confirmed by pull-down/mass spectrometry, co-immunoprecipitation, and immunofluorescence; YWHAG upregulates TMOD3 expression, which activates ERK1/2 and JNK phosphorylation in the MAPK pathway to promote bladder cancer cell invasion and metastasis. Pull-down with mass spectrometry, co-immunoprecipitation, immunofluorescence, transcriptome sequencing, TMOD3 knockdown rescue experiment, in vitro invasion assays Journal of translational medicine Medium 39741303
2019 14-3-3γ localizes specifically to pseudopodia of breast cancer cells and promotes cancer cell motility; knockdown reduces pseudopodial formation and elongation as well as migration, while forced expression increases them. Confocal imaging of 14-3-3γ in pseudopodia (excimer laser cell etching isolation), siRNA knockdown and overexpression, wound healing and Transwell migration assays Breast cancer (Tokyo, Japan) Medium 30830684
2014 p53 interacts with the C-terminal domain of 14-3-3γ and induces its ubiquitination, stimulating proteasome-mediated degradation of 14-3-3γ; MG132 blocks this effect. Wild-type but not R175H mutant p53 suppresses 14-3-3γ. Co-immunoprecipitation of p53 and 14-3-3γ, ubiquitination assay, proteasome inhibitor (MG132), mutant p53 comparison International journal of oncology Medium 25384678
2015 USP37 (deubiquitinating enzyme) binds 14-3-3γ and regulates its stability by deubiquitinating it through its catalytic activity, preventing 14-3-3γ degradation and thereby contributing to oncogenic MAPK signaling. Co-immunoprecipitation, ubiquitination assay, USP37 catalytic mutant, cell proliferation and transformation assays Oncotarget Medium 26427597
2023 YWHAG (14-3-3γ) supports a cytoprotective mechanism during EMT by enhancing autophagy, protecting cancer cells from oxidative catastrophe (ROS accumulation) during the EMT process. YWHAG deficiency results in rapid ROS accumulation, delayed EMT, and cancer cell death. Metastasized tumors express higher YWHAG and autophagy-related genes than primary tumors. YWHAG knockdown/deficiency, cellular kinome and transcriptome profiling, ROS measurement, tumor allograft model with survival analysis, autophagy flux assay Advanced science Medium 37759388
2021 YWHAG missense mutations in the 14-3-3γ binding groove (9 mutations) or dimerization residues (1 mutation) cause epileptic encephalopathy; the Arg132Cys mutation (recurrent in 5 EE patients) most strongly affects binding affinity. Heterozygous missense mutations lead to a predominance of mutant dimers, while truncating mutations reduce wild-type dimer number, explaining phenotypic variation. Trio-based whole exome sequencing, molecular sub-regional analysis mapping mutations to binding groove vs. dimerization domains, genotype-phenotype correlation in human patients Frontiers in genetics Medium 33767733
2022 miR-200c regulates 14-3-3γ (YWHAG) translation in hippocampal neurons; miR-200c inhibition increases 14-3-3γ protein levels and tau phosphorylation via increased p-GSK-3β activity. miR-200c inhibition in mouse hippocampus induces cognitive impairment and tau hyperphosphorylation through 14-3-3γ activation. Dual-luciferase assay confirming miR-200c targeting of Ywhag 3'UTR, miR-200c inhibitor in primary neurons and C57BL/6J mice, p-GSK-3β and p-tau Western blot, behavioral testing International journal of biological sciences Medium 35342350
2019 14-3-3γ is required for starvation-activated neuronal autophagic influx; upon starvation, 14-3-3γ binds more p-β-catenin and less Beclin-1, releasing Beclin-1 to activate LC3-dependent autophagy. Only the γ isoform (not other 14-3-3 isoforms) upregulates Beclin-1-LC3 signaling; 14-3-3γ knockout abolishes starvation-induced Beclin-1 induction. Co-immunoprecipitation (14-3-3γ with p-β-catenin and Beclin-1), isoform-specific knockout, overexpression of individual 14-3-3 isoforms, double-fluorescent immunostaining in ischemic brains, autophagy flux assay Neurochemical research Medium 30635843
2024 YWHAG interacts with CTTN (cortactin) and mediates activation of Wnt/β-catenin signaling to promote colorectal cancer cell proliferation, migration, and invasion. RNA-seq, co-immunoprecipitation (CTTN as YWHAG-associated protein), YWHAG knockdown, Wnt/β-catenin pathway analysis, in vitro proliferation/invasion assays Medical oncology Low 38538804

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 Curcumin attenuates doxorubicin-induced cardiotoxicity via suppressing oxidative stress and preventing mitochondrial dysfunction mediated by 14-3-3γ. Food & function 102 30063064
2006 14-3-3gamma binds to MDMX that is phosphorylated by UV-activated Chk1, resulting in p53 activation. The EMBO journal 100 16511572
2003 A dual role for poly-ADP-ribosylation in spatial memory acquisition after traumatic brain injury in mice involving NAD+ depletion and ribosylation of 14-3-3gamma. Journal of neurochemistry 87 12694396
2010 14-3-3gamma mediates Cdc25A proteolysis to block premature mitotic entry after DNA damage. The EMBO journal 74 20639859
2012 A 14-3-3γ dimer-based scaffold bridges CtBP1-S/BARS to PI(4)KIIIβ to regulate post-Golgi carrier formation. Nature cell biology 72 22366688
2006 Small heat shock protein Hsp20 (HspB6) as a partner of 14-3-3gamma. Molecular and cellular biochemistry 68 17109079
2016 miR-181b-3p promotes epithelial-mesenchymal transition in breast cancer cells through Snail stabilization by directly targeting YWHAG. Biochimica et biophysica acta 63 27102539
2013 PI 3-kinase-dependent phosphorylation of Plk1-Ser99 promotes association with 14-3-3γ and is required for metaphase-anaphase transition. Nature communications 60 23695676
2005 Unchanged survival rates of 14-3-3gamma knockout mice after inoculation with pathological prion protein. Molecular and cellular biology 59 15684385
2017 De Novo Mutations in YWHAG Cause Early-Onset Epilepsy. American journal of human genetics 58 28777935
2005 Role of 14-3-3gamma in FE65-dependent gene transactivation mediated by the amyloid beta-protein precursor cytoplasmic fragment. The Journal of biological chemistry 57 16223726
2010 Recurrent distal 7q11.23 deletion including HIP1 and YWHAG identified in patients with intellectual disabilities, epilepsy, and neurobehavioral problems. American journal of human genetics 56 21109226
2019 Quercetin protects cardiomyocytes against doxorubicin-induced toxicity by suppressing oxidative stress and improving mitochondrial function via 14-3-3γ. Toxicology mechanisms and methods 55 30636491
2003 14-3-3gamma is upregulated by in vitro ischemia and binds to protein kinase Raf in primary cultures of astrocytes. Glia 47 12730952
2017 PAK6 Phosphorylates 14-3-3γ to Regulate Steady State Phosphorylation of LRRK2. Frontiers in molecular neuroscience 45 29311810
2016 Suppression of 14-3-3γ-mediated surface expression of ANO1 inhibits cancer progression of glioblastoma cells. Scientific reports 44 27212225
2006 14-3-3gamma affects dynamics and integrity of glial filaments by binding to phosphorylated GFAP. Journal of cell science 43 17032734
2010 14-3-3gamma induces oncogenic transformation by stimulating MAP kinase and PI3K signaling. PloS one 42 20628654
2005 Association of 14-3-3gamma and phosphorylated bad attenuates injury in ischemic astrocytes. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 42 15660102
2016 MiR-509-5p suppresses the proliferation, migration, and invasion of non-small cell lung cancer by targeting YWHAG. Biochemical and biophysical research communications 39 27894843
2009 Ischemia activates JNK/c-Jun/AP-1 pathway to up-regulate 14-3-3gamma in astrocyte. Journal of neurochemistry 39 19393026
2021 LncRNA CERS6-AS1 promotes proliferation and metastasis through the upregulation of YWHAG and activation of ERK signaling in pancreatic cancer. Cell death & disease 38 34168120
2009 Silencing neuroglobin enhances neuronal vulnerability to oxidative injury by down-regulating 14-3-3gamma. Acta pharmacologica Sinica 38 19574997
2007 Overexpression of 14-3-3gamma causes polyploidization in H322 lung cancer cells. Molecular carcinogenesis 38 17394238
2017 Elevation of adenylate energy charge by angiopoietin-like 4 enhances epithelial-mesenchymal transition by inducing 14-3-3γ expression. Oncogene 36 28745316
2014 14-3-3γ protein attenuates lipopolysaccharide-induced cardiomyocytes injury through the Bcl-2 family/mitochondria pathway. International immunopharmacology 36 24957688
2021 Capsaicin protects cardiomyocytes against lipopolysaccharide-induced damage via 14-3-3γ-mediated autophagy augmentation. Frontiers in pharmacology 35 33986684
2012 Hormone-induced 14-3-3γ adaptor protein regulates steroidogenic acute regulatory protein activity and steroid biosynthesis in MA-10 Leydig cells. The Journal of biological chemistry 35 22427666
2002 The association of 14-3-3gamma and actin plays a role in cell division and apoptosis in astrocytes. Biochemical and biophysical research communications 34 12176032
2021 Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG. Bioengineered 32 34709972
2020 Emerging roles of 14-3-3γ in the brain disorder. BMB reports 32 32958119
2010 Zebrafish gene knockdowns imply roles for human YWHAG in infantile spasms and cardiomegaly. Genesis (New York, N.Y. : 2000) 32 20146355
2022 Puerarin activates adaptive autophagy and protects the myocardium against doxorubicin-induced cardiotoxicity via the 14-3-3γ/PKCε pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 31 36076529
2018 Tetramethylpyrazine attenuates lipopolysaccharide-induced cardiomyocyte injury via improving mitochondrial function mediated by 14-3-3γ. European journal of pharmacology 31 29782860
2018 Preconditioning exercise reduces brain damage and neuronal apoptosis through enhanced endogenous 14-3-3γ after focal brain ischemia in rats. Brain structure & function 31 30478609
2017 MiR-217 promoted the proliferation and invasion of glioblastoma by repressing YWHAG. Cytokine 31 28126486
1999 14-3-3Gamma interacts with and is phosphorylated by multiple protein kinase C isoforms in PDGF-stimulated human vascular smooth muscle cells. DNA and cell biology 31 10433554
2016 14-3-3γ Prevents Centrosome Amplification and Neoplastic Progression. Scientific reports 29 27253419
2014 Depletion of 14-3-3γ reduces the surface expression of Transient Receptor Potential Melastatin 4b (TRPM4b) channels and attenuates TRPM4b-mediated glutamate-induced neuronal cell death. Molecular brain 28 25047048
2010 14-3-3gamma and neuroglobin are new intrinsic protective factors for cerebral ischemia. Molecular neurobiology 28 20467836
2019 Tetramethylpyrazine Attenuates the Endotheliotoxicity and the Mitochondrial Dysfunction by Doxorubicin via 14-3-3γ/Bcl-2. Oxidative medicine and cellular longevity 27 31885804
2015 14-3-3γ Regulates Lipopolysaccharide-Induced Inflammatory Responses and Lactation in Dairy Cow Mammary Epithelial Cells by Inhibiting NF-κB and MAPKs and Up-Regulating mTOR Signaling. International journal of molecular sciences 27 26204835
2014 Selective 14-3-3γ induction quenches p-β-catenin Ser37/Bax-enhanced cell death in cerebral cortical neurons during ischemia. Cell death & disease 27 24743739
2015 Ablation of the 14-3-3gamma Protein Results in Neuronal Migration Delay and Morphological Defects in the Developing Cerebral Cortex. Developmental neurobiology 26 26297819
2015 Deubiquitinating enzyme USP37 regulating oncogenic function of 14-3-3γ. Oncotarget 26 26427597
2010 Involvement of 14-3-3γ overexpression in extrahepatic metastasis of hepatocellular carcinoma. Human pathology 26 20870266
1999 Cloning, expression, and chromosomal mapping of the human 14-3-3gamma gene (YWHAG) to 7q11.23. Genomics 26 10486217
2022 miR-200c suppression increases tau hyperphosphorylation by targeting 14-3-3γ in early stage of 5xFAD mouse model of Alzheimer's disease. International journal of biological sciences 24 35342350
2021 YWHAG Mutations Cause Childhood Myoclonic Epilepsy and Febrile Seizures: Molecular Sub-regional Effect and Mechanism. Frontiers in genetics 23 33767733
2014 Molecular network including eIF1AX, RPS7, and 14-3-3γ regulates protein translation and cell proliferation in bovine mammary epithelial cells. Archives of biochemistry and biophysics 23 25281768
2016 Sporadic Creutzfeldt-Jakob disease diagnostic accuracy is improved by a new CSF ELISA 14-3-3γ assay. Neuroscience 22 26940479
2012 Hypoxia activates tumor suppressor p53 by inducing ATR-Chk1 kinase cascade-mediated phosphorylation and consequent 14-3-3γ inactivation of MDMX protein. The Journal of biological chemistry 21 22556425
2023 YWHAG Deficiency Disrupts the EMT-Associated Network to Induce Oxidative Cell Death and Prevent Metastasis. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20 37759388
2020 Functional genetic variants in centrosome-related genes CEP72 and YWHAG confer susceptibility to gastric cancer. Archives of toxicology 20 32535685
2014 Protein modifications regulate the role of 14-3-3γ adaptor protein in cAMP-induced steroidogenesis in MA-10 Leydig cells. The Journal of biological chemistry 20 25086053
2015 Mitotic Golgi translocation of ERK1c is mediated by a PI4KIIIβ-14-3-3γ shuttling complex. Journal of cell science 19 26459638
2014 14-3-3γ-Mediated transport of plakoglobin to the cell border is required for the initiation of desmosome assembly in vitro and in vivo. Journal of cell science 19 24610948
2014 Phosphorylation dependence and stoichiometry of the complex formed by tyrosine hydroxylase and 14-3-3γ. Molecular & cellular proteomics : MCP 19 24947669
2016 YAP and 14-3-3γ are involved in HS-OA-induced growth inhibition of hepatocellular carcinoma cells: A novel mechanism for hydrogen sulfide releasing oleanolic acid. Oncotarget 18 27437776
2012 The peripheral binding of 14-3-3γ to membranes involves isoform-specific histidine residues. PloS one 17 23189152
2010 14-3-3Gamma inhibition of MDMX-mediated p21 turnover independent of p53. The Journal of biological chemistry 17 21148311
2019 Breast cancer cell motility is promoted by 14-3-3γ. Breast cancer (Tokyo, Japan) 16 30830684
2016 Overexpression of the 14-3-3gamma protein in embryonic mice results in neuronal migration delay in the developing cerebral cortex. Neuroscience letters 16 27288018
2015 Protein kinase CK2 interacts at the neuromuscular synapse with Rapsyn, Rac1, 14-3-3γ, and Dok-7 proteins and phosphorylates the latter two. The Journal of biological chemistry 16 26198629
2018 14-3-3γ binds regulator of G protein signaling 14 (RGS14) at distinct sites to inhibit the RGS14:Gαi-AlF4- signaling complex and RGS14 nuclear localization. The Journal of biological chemistry 15 30093406
2004 Inducible expression of the signal transduction protein 14-3-3gamma in injured arteries and stimulated human vascular smooth muscle cells. Experimental and molecular pathology 15 15010287
2022 Curcumenol Targeting YWHAG Inhibits the Pentose Phosphate Pathway and Enhances Antitumor Effects of Cisplatin. Evidence-based complementary and alternative medicine : eCAM 14 35795276
2018 Knockdown of 14-3-3γ Suppresses Epithelial-Mesenchymal Transition and Reduces Metastatic Potential of Human Non-small Cell Lung Cancer Cells. Anticancer research 14 29848704
2013 Quantitative proteome analysis of overexpressed Cripto-1 tumor cell reveals 14-3-3γ as a novel biomarker in nasopharyngeal carcinoma. Journal of proteomics 14 23500129
2013 Induction of activation-induced cytidine deaminase-targeting adaptor 14-3-3γ is mediated by NF-κB-dependent recruitment of CFP1 to the 5'-CpG-3'-rich 14-3-3γ promoter and is sustained by E2A. Journal of immunology (Baltimore, Md. : 1950) 14 23851690
2016 14-3-3γ regulates cell viability and milk fat synthesis in lipopolysaccharide-induced dairy cow mammary epithelial cells. Experimental and therapeutic medicine 13 27073437
2017 14-3-3γ regulates Copine1-mediated neuronal differentiation in HiB5 hippocampal progenitor cells. Experimental cell research 12 28412242
2017 Direct interaction with 14-3-3γ promotes surface expression of Best1 channel in astrocyte. Molecular brain 12 29121962
2015 14-3-3γ affects mTOR pathway and regulates lactogenesis in dairy cow mammary epithelial cells. In vitro cellular & developmental biology. Animal 12 26183263
2022 Puerarin attenuates lipopolysaccharide-induced myocardial injury via the 14-3-3γ/PKCε pathway activating adaptive autophagy. International immunopharmacology 11 35729836
2020 A histone deacetylase 7-derived peptide promotes vascular regeneration via facilitating 14-3-3γ phosphorylation. Stem cells (Dayton, Ohio) 11 31721359
2019 Selective 14-3-3γ Upregulation Promotes Beclin-1-LC3-Autophagic Influx via β-Catenin Interaction in Starved Neurons In Vitro and In Vivo. Neurochemical research 11 30635843
2015 Ischemia preconditioning protects astrocytes from ischemic injury through 14-3-3γ. Journal of neuroscience research 11 25711139
2012 Activation of phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling and the consequent induction of transformation by overexpressed 14-3-3γ protein require specific amino acids within 14-3-3γ N-terminal variable region II. The Journal of biological chemistry 11 23115241
2019 miR-140-5p mediates bevacizumab-induced cytotoxicity to cardiomyocytes by targeting the VEGFA/14-3-3γ signal pathway. Toxicology research 10 32190292
2018 MicroRNA-222 contributed to cell proliferation, invasion and migration via regulating YWHAG in osteosarcoma. European review for medical and pharmacological sciences 10 29771442
2012 Identification of 14-3-3γ as a Mieap-interacting protein and its role in mitochondrial quality control. Scientific reports 10 22532927
2021 Epilepsy and electroencephalogram evolution in YWHAG gene mutation: A new phenotype and review of the literature. American journal of medical genetics. Part A 8 33393734
2014 p53 suppresses 14-3-3γ by stimulating proteasome-mediated 14-3-3γ protein degradation. International journal of oncology 8 25384678
2023 14-3-3γ haploinsufficiency leads to altered dopamine pathway and Parkinson's disease-like motor incoordination in mice. Molecular brain 7 36604743
2020 Identification of Sec23ip, Part of 14-3-3γ Protein Network, as a Regulator of Acute Steroidogenesis in MA-10 Leydig Cells. Endocrinology 7 31875919
2018 Overexpression of the 14-3-3γ protein in uterine leiomyoma cells results in growth retardation and increased apoptosis. Cellular signalling 7 29382566
2018 MicroRNA-182 promoted esophageal squamous cell carcinoma cell growth and metastasis via targeting YWHAG. Journal of B.U.ON. : official journal of the Balkan Union of Oncology 7 30570871
2012 Superhelical DNA as a preferential binding target of 14-3-3γ protein. Journal of biomolecular structure & dynamics 7 22856523
2024 Serum level of YWHAG as a diagnostic marker of cognitive impairment in Parkinson's disease patients. Acta neurologica Belgica 6 38286872
2024 YWHAG promotes colorectal cancer progression by regulating the CTTN-Wnt/β-catenin signaling axis. Medical oncology (Northwood, London, England) 6 38538804
2024 YWHAG promotes bladder cancer metastasis by regulating TMOD3 to activate ERK1/2 and JNK phosphorylation in the MAPK pathway. Journal of translational medicine 6 39741303
2022 TXNDC9 knockdown inhibits lung adenocarcinoma progression by targeting YWHAG. Molecular medicine reports 6 35485284
2022 A heterozygous missense variant in the YWHAG gene causing developmental and epileptic encephalopathy 56 in a Chinese family. BMC medical genomics 6 36243722
2017 Plakoglobin localization to the cell border restores desmosome function in cells lacking 14-3-3γ. Biochemical and biophysical research communications 6 29253567
2025 Thymoquinone mitigates cardiac hypertrophy by activating adaptive autophagy via the PPAR‑γ/14‑3‑3γ pathway. International journal of molecular medicine 5 39918010
2024 Prospective Role of PAK6 and 14-3-3γ as Biomarkers for Parkinson's Disease. Journal of Parkinson's disease 5 38640169
2021 Disruption of desmosome function leads to increased centrosome clustering in 14-3-3γ-knockout cells with supernumerary centrosomes. FEBS letters 5 34626438
2021 LncRNA PTPRG-AS1 Promotes the Metastasis of Hepatocellular Carcinoma by Enhancing YWHAG. Journal of oncology 5 34876904
2017 The induction of endoreduplication and polyploidy by elevated expression of 14-3-3γ. Genes & cancer 4 29321819