Affinage

EIF3E

Eukaryotic translation initiation factor 3 subunit E · UniProt P60228

Length
445 aa
Mass
52.2 kDa
Annotated
2026-06-09
40 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

EIF3E (eIF3e/INT6/p48) is a non-core subunit of the eIF3 translation initiation complex that couples general translation initiation to selective, regulated translation of defined mRNA subsets (PMID:9295280, PMID:15904532). It integrates into eIF3 by binding directly to eIF3b and is required to maintain inter-subunit cohesion of the eIF3 complex after ribosome dissociation (PMID:11457827, PMID:11705997). As the eIF4G-binding subunit of mammalian eIF3, eIF3e bridges eIF3 to the cap-binding apparatus, and an excess of free eIF3e competes for eIF4G-1 and inhibits cap-dependent initiation (PMID:16766523). Rather than driving bulk protein synthesis, eIF3e specializes in translational control of particular transcripts and can promote cap-independent initiation: C-terminal truncation mimicking MMTV integration weakens eIF3–eIF4G binding, shifts the balance from cap-dependent to IRES-driven translation, and causes malignant transformation (PMID:11904180, PMID:21737453). eIF3e directs translation of specific targets including BCL-XL, urokinase plasminogen activator, PARP1 and HIF1α, and assembles a selective eIF3E–eIF4G1–mRNA complex that translates GAGGACR-motif mRNAs (TFRC, ACSL4, UAP1) when released from inhibitory ALDH2 binding, driving cardiomyocyte ferroptosis (PMID:20453879, PMID:33868586, PMID:41111418, PMID:41364558). Loss of eIF3e induces epithelial-to-mesenchymal transition through TGFβ overproduction and HIF2α–TWIST1-mediated repression of E-cadherin (PMID:22907435, PMID:26056130, PMID:36116043). Beyond translation, eIF3e functions in nonsense-mediated mRNA decay via association with CBP80 and UPF2 (PMID:17468741), promotes ATM–RNF8–BRCA1-dependent homologous-recombination repair of DNA double-strand breaks (PMID:22508697, PMID:27550454), mediates activity-dependent endocytosis of the CaV1.2 calcium channel (PMID:17698014), and acts as a translational checkpoint maintaining B-cell immune tolerance (PMID:42233886). eIF3e abundance is controlled by TRIM35-mediated ubiquitination and degradation (PMID:41429342).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1997 High

    Established that the 48-kDa eIF3 subunit is a defined gene product physically embedded in the translation initiation complex, fixing EIF3E's foundational identity.

    Evidence cDNA cloning, recombinant expression, and co-IP with anti-eIF3 p170 antibodies

    PMID:9295280

    Open questions at the time
    • Did not define which subunit contacts mediate integration
    • No functional role beyond complex membership
  2. 2001 High

    Resolved how eIF3e physically enters eIF3 and whether it is structurally required, showing a direct eIF3b interface and a role in holding the complex together.

    Evidence Yeast in vivo/in vitro binding and domain mapping (eIF3b interaction); fission yeast int6 deletion with ribosome fractionation

    PMID:11457827 PMID:11705997

    Open questions at the time
    • Structural basis of the eIF3b-eIF3e interface not solved
    • Did not address mRNA selectivity
  3. 2005 High

    Reframed eIF3e from a generic initiation factor to a specialized regulator by showing it is dispensable for global translation but governs a restricted mRNA set.

    Evidence Fission yeast genetic deletion, polysome analysis, and ribonomic mRNA-association profiling

    PMID:15904532

    Open questions at the time
    • Identity of the selected mRNAs in mammals not defined
    • Mechanism of selectivity unknown
  4. 2006 High

    Identified the molecular link between eIF3e and the cap-binding machinery, defining eIF3e as the eIF4G-1-binding subunit whose stoichiometry tunes cap-dependent initiation.

    Evidence Competitive in vitro binding, cell-free translation, and polysome profiling

    PMID:16766523

    Open questions at the time
    • How physiological eIF3e levels are regulated to set initiation balance not addressed
    • Binding interface on eIF4G-1 mapped only functionally
  5. 2002 High

    Connected eIF3e structural perturbation to cancer, showing that a C-terminally truncated form is a transforming gain-of-function variant.

    Evidence Stable expression of truncated vs full-length eIF3e in NIH 3T3 with transformation and apoptosis assays

    PMID:11904180

    Open questions at the time
    • Molecular mechanism of transformation not resolved at this stage
    • In vivo tumorigenicity not tested
  6. 2011 High

    Provided the mechanistic explanation for truncation-driven oncogenesis by showing the truncated form weakens eIF3–eIF4G binding and shifts translation toward cap-independent mRNAs.

    Evidence Single-copy knockin cell line, co-IP, bicistronic IRES reporter, polysome profiling (XIAP, c-Myc, CYR61, Pim-1)

    PMID:21737453

    Open questions at the time
    • How cap-independent mRNAs are selected not defined
    • Link between specific targets and transformation incomplete
  7. 2007 High

    Extended eIF3e function beyond initiation, revealing roles in NMD and in membrane-channel trafficking.

    Evidence siRNA NMD reporter assays and co-IP with CBP80/UPF2; co-IP, TIRF imaging and domain mutagenesis of CaV1.2 internalization

    PMID:17468741 PMID:17698014

    Open questions at the time
    • Whether NMD and channel-trafficking roles require eIF3 complex membership unclear
    • Mechanism linking eIF3e to UPF1/UPF2 step undefined
  8. 2008 High

    Demonstrated that eIF3e supports stress-responsive gene expression by maintaining translation of a stress MAPK target, linking it to adaptive signaling.

    Evidence Fission yeast pulse-labeling, protein half-life, and genetic epistasis with sty1Δ/gcn2Δ (Atf1 levels)

    PMID:18502752

    Open questions at the time
    • Mammalian equivalent of Atf1 control not established
    • Direct vs indirect effect on Atf1 mRNA unresolved
  9. 2010 Medium

    Defined specific mammalian translational targets of eIF3e, confirming selective rather than bulk translational control in cancer cells.

    Evidence siRNA knockdown with total vs polysomal microarray and target validation (uPA, BCL-XL, MAD2L1)

    PMID:20453879

    Open questions at the time
    • Sequence/structural features driving target selection not identified
    • Single-lab dataset
  10. 2012 High

    Established eIF3e as a DNA double-strand break repair factor acting in the ATM signaling axis, distinct from its translational role; concurrent work showed viral hijacking of its NMD function.

    Evidence Co-IP (INT6–ATM), RNAi, damage-site immunofluorescence, CHK1/CHK2 phosphorylation; HTLV-1 Tax co-IP and NMD reporter assays

    PMID:22508697 PMID:22553336

    Open questions at the time
    • How a translation factor is recruited to chromatin damage sites unknown
    • Whether repair role is eIF3-dependent unclear
  11. 2012 Medium

    Linked eIF3e loss to a tumor-relevant EMT program, identifying Snail1 and Zeb2 as induced effectors.

    Evidence siRNA knockdown in MCF-10A with EMT marker, invasion/migration assays and Snail1/Zeb2 quantification

    PMID:22907435

    Open questions at the time
    • Direct vs indirect control of Snail1/Zeb2 not fully separated
    • Single cell-line model
  12. 2015 Medium

    Identified TGFβ as the causal mediator of eIF3e-loss-driven EMT and tied EMT regulators to cap-independent translation.

    Evidence shRNA knockdown, TGFβ ELISA, TGFβ inhibitor rescue, polysomal cap-independence analysis in A549

    PMID:26056130

    Open questions at the time
    • Which EMT mRNAs use cap-independent initiation not exhaustively mapped
    • Single lab
  13. 2016 High

    Refined the DSB-repair mechanism, placing eIF3e upstream of RNF8-dependent K63 ubiquitination and BRCA1/BRCA2/RAD51 recruitment in homologous recombination.

    Evidence RNAi, laser-induced DSB immunofluorescence, ubiquitin chain analysis, HR repair assay with RNF168/53BP1 controls

    PMID:27550454

    Open questions at the time
    • Direct molecular target of eIF3e at damage sites unidentified
    • Whether effect is translational or structural unresolved
  14. 2021 Medium

    Connected eIF3e translational control to cellular senescence through PARP1 translation and mTORC1 regulation.

    Evidence siRNA knockdown, PARP1 polysome profiling, mTORC1 activity, SA-β-gal/SASP senescence assays

    PMID:33868586

    Open questions at the time
    • Mechanism of mTORC1 dysregulation not defined
    • Single lab
  15. 2022 Medium

    Identified HIF2α stability as an eIF3e-regulated node driving EMT via TWIST1 and E-cadherin repression.

    Evidence siRNA knockdown, HIF2α western blotting, HIF2α–TWIST1 co-IP, E-cadherin promoter ChIP

    PMID:36116043

    Open questions at the time
    • How eIF3e controls oxygen-independent HIF2α stability mechanistically unknown
    • Single lab
  16. 2024 Medium

    Established eIF3e abundance as a regulated quantity through TRIM35-mediated ubiquitination and degradation affecting proliferation.

    Evidence Co-IP, ubiquitination assay, lentiviral perturbation, rescue, CDK4/Cyclin D1 western blotting

    PMID:41429342

    Open questions at the time
    • Ubiquitination site and chain type on eIF3E not defined
    • Single lab
  17. 2024 Medium

    Revealed a non-canonical RNA-binding function of eIF3e distinct from initiation, binding the TLR7 3'UTR to upregulate TLR7 in myeloma.

    Evidence RNA immunoprecipitation / 3'UTR binding, REIIBP perturbation, TLR7 quantification

    PMID:38124661

    Open questions at the time
    • Whether 3'UTR binding is direct and sequence-specific genome-wide unknown
    • Single lab
  18. 2025 High

    Provided a mechanistic model for selective translation, showing ALDH2 sequesters eIF3e and its release enables a GAGGACR-motif-driven eIF3E–eIF4G1–mRNA program causing cardiomyocyte ferroptosis, while a parallel study tied eIF3e/eIF3d to hypoxia- and ER-stress-selective translation controlling HIF1α.

    Evidence ALDH2–eIF3E co-IP, cardiomyocyte AAV knockdown in mice, lipidomics, motif analysis; ribosome profiling with siRNA and small-molecule eIF3e inhibition

    PMID:41111418 PMID:41364558

    Open questions at the time
    • How the GAGGACR motif is recognized structurally not resolved
    • Breadth of the selective translatome across tissues unknown
  19. 2026 Medium

    Defined eIF3e as a translational checkpoint enforcing immune tolerance, with B-cell deletion triggering a feedforward hyperactivation loop and lymphocyte transformation.

    Evidence Conditional Cγ1Cre-Eif3e knockout mice, flow cytometry, B/T co-culture, IL-4 quantification

    PMID:42233886

    Open questions at the time
    • Specific mRNAs whose translation enforces tolerance not identified
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How eIF3e physically recognizes its selective mRNA targets (e.g., the GAGGACR motif) and how it is partitioned between canonical eIF3-dependent initiation, cap-independent translation, NMD, DSB repair and RNA-binding roles remains unresolved.
  • No structure of an eIF3e–mRNA selective complex
  • Recruitment mechanism to DNA damage sites undefined
  • Unclear whether non-translational roles require eIF3 membership

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0045182 translation regulator activity 7 GO:0060090 molecular adaptor activity 3 GO:0003723 RNA binding 2
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2
Pathway
R-HSA-73894 DNA Repair 2 R-HSA-8953854 Metabolism of RNA 2
Partners
ALDH2ATMCACNA1CCBP80EIF3BEIF4G1TRIM35UPF2
Complex memberships
eIF3

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 EIF3E (eIF3-p48/Int-6) was identified as the 48-kDa subunit of the eIF3 translation initiation complex; recombinant eIF3-p48 comigrates with the authentic p48 subunit in purified eIF3 and co-precipitates with affinity-purified antibodies to the eIF3 p170 subunit, establishing its membership in the eIF3 complex. CDNA cloning, recombinant protein expression, co-immunoprecipitation with anti-p170 antibodies The Journal of biological chemistry High 9295280
2001 Human eIF3e/Int-6 binds directly to eIF3b (Prt1p in yeast) through a discrete segment of eIF3b, establishing the molecular basis for eIF3e integration into the eIF3 core complex; this interaction was demonstrated both in vivo and in vitro in a budding yeast expression system. In vivo and in vitro binding assays in S. cerevisiae, yeast two-hybrid, domain mapping The Journal of biological chemistry High 11457827
2001 In fission yeast, spInt6 (eIF3e homologue) is required for stable association of eIF3 subunits after dissociation from ribosomes; deletion of int6 results in loss of inter-subunit eIF3 cohesion while eIF3 subunits remain bound to 40S particles, demonstrating a structural role of eIF3e in maintaining eIF3 complex integrity. Genetic deletion, ribosome fractionation, co-purification of eIF3 subunits from 40S particles The Journal of biological chemistry High 11705997
2005 In fission yeast, eIF3e defines a distinct eIF3 complex (separate from the eIF3m complex) that associates with a restricted subset of cellular mRNAs; eIF3e is non-essential for global protein synthesis whereas eIF3m is essential, indicating eIF3e specializes in translational regulation of specific mRNAs. Genetic deletion, polysome analysis, ribonomic mRNA-association profiling (microarray + RT-PCR) BMC biology High 15904532
2006 eIF3e directly binds eIF4G-1 and constitutes the eIF4G-binding subunit of mammalian eIF3; recombinant FLAG-eIF3e competes with intact eIF3 for binding to the eIF3-binding domain of eIF4G-1 in vitro, and excess eIF3e inhibits cap-dependent translation, shifts mRNA to lighter polysomes, and displaces eIF4G and eIF2α from ~40S complexes. Proteolysis/mass spectrometry-based binding assay, competitive in vitro binding, cell-free translation system, polysome profiling The Journal of biological chemistry High 16766523
2002 Stable expression of a C-terminally truncated eIF3e (mimicking MMTV integration) in NIH 3T3 cells causes malignant transformation (foci formation, anchorage-independent growth, accelerated growth, loss of contact inhibition) and inhibits apoptosis onset; full-length eIF3e does not cause transformation, indicating the truncated form acts as a dominant-negative/oncogenic variant. Stable transfection of truncated vs. full-length eIF3e, transformation assays (foci, soft agar, growth curves), apoptosis assay FEBS letters High 11904180
2004 eIF3e/INT6 localizes partly to the nucleus in human primary fibroblasts, with reduced nuclear staining specifically in early S phase, indicating cell cycle-regulated nucleocytoplasmic shuttling; transformed cells lose this regulated redistribution, suggesting it is relevant to tumor suppressor function. Immunofluorescence microscopy, cell cycle synchronization Cell proliferation Medium 15030549
2007 eIF3e/Int6 mediates activity-dependent internalization of the L-type calcium channel CaV1.2 by binding to a domain in the II-III loop of CaV1.2; electrical activity triggers CaV1.2 endocytosis and rapid endosomal trafficking in a Ca2+-dependent manner, and the eIF3e-binding domain in CaV1.2 is essential for this internalization. Co-immunoprecipitation, total internal reflection microscopy (TIRF), domain deletion mutagenesis, live-cell imaging of endosomal trafficking Neuron High 17698014
2007 INT6/eIF3e is required for nonsense-mediated mRNA decay (NMD); INT6 knockdown strongly inhibits NMD without affecting general translation (unlike eIF3b knockdown). INT6 co-immunoprecipitates with the cap-binding protein CBP80 and the NMD factor UPF2, placing INT6 in the NMD pathway upstream of mRNA degradation. siRNA knockdown, NMD reporter assays, co-immunoprecipitation with CBP80 and UPF2, NMD-sensitive transcript quantification EMBO reports High 17468741
2008 In fission yeast, Int6/eIF3e promotes general translation and maintains basal Atf1 (a Sty1 MAPK target transcription factor) protein levels; int6Δ slows de novo protein synthesis (pulse labeling) and reduces Atf1 protein half-life, thereby impairing Sty1 MAPK-dependent stress response to amino acid starvation. Pulse-labeling translation assay, northern/microarray analysis, protein half-life measurement, genetic epistasis with sty1Δ and gcn2Δ The Journal of biological chemistry High 18502752
2010 eIF3e is not required for bulk translation in breast cancer cells, but regulates translation of specific mRNAs including positive regulation of urokinase-type plasminogen activator and BCL-XL, and negative regulation of MAD2L1, as determined by microarray comparison of total vs. polysomal RNA after siRNA-mediated eIF3e knockdown. siRNA knockdown, microarray of total and polysomal RNA fractions, validation of specific targets Oncogene Medium 20453879
2011 Expression of truncated eIF3e (3e5, resulting from MMTV integration at intron 5) diminishes binding of eIF3 to eIF4G (co-IP), reduces overall protein synthesis and cell growth, increases cap-independent IRES-driven translation relative to cap-dependent translation, and shifts endogenous cap-independent mRNAs (XIAP, c-Myc, CYR61, Pim-1) to heavier polysomes while cap-dependent mRNAs shift to lighter polysomes. Co-immunoprecipitation, bicistronic IRES reporter assay, polysome profiling, single-copy knockin cell line The Journal of biological chemistry High 21737453
2012 HTLV-1 Tax protein inhibits NMD by binding to INT6/eIF3e and UPF1; Tax interaction with INT6 is necessary for NMD inhibition, as shown by Tax mutant analysis. Tax expression decreases INT6 abundance in P-bodies and increases phosphorylated UPF1, collectively impairing NMD of viral and cellular transcripts. Co-immunoprecipitation, Tax mutant analysis, P-body morphology and marker quantification, NMD reporter assays, western blotting Journal of virology High 22553336
2012 INT6/eIF3e interacts with ATM kinase and is recruited to DNA damage sites; INT6 silencing reduces ATM retention at damage sites, impairs CHK1/CHK2 phosphorylation, attenuates ubiquitylation (K63-linked polyubiquitin) at DSBs, and prevents BRCA1 accumulation at damage sites, placing INT6 in the ATM-RNF8-BRCA1 DSB repair pathway. Co-immunoprecipitation (INT6–ATM), RNAi silencing, γ-H2AX foci, immunofluorescence of ATM/BRCA1 at damage sites, western blotting of CHK1/CHK2 phosphorylation, γ-irradiation/neocarzinostatin treatment Cancer research High 22508697
2012 Decreased eIF3e expression in MCF-10A breast epithelial cells induces epithelial-to-mesenchymal transition (EMT) and increases invasion/migration; reduced eIF3e causes specific upregulation of EMT regulators Snail1 and Zeb2 at both transcriptional and post-transcriptional levels. siRNA knockdown, EMT marker analysis, invasion/migration assays, qRT-PCR and western blotting for Snail1/Zeb2 Oncogene Medium 22907435
2015 Decreased eIF3e expression induces EMT in lung epithelial cells (A549) via overproduction of TGFβ cytokine; inhibition of TGFβ signaling reverses eIF3e-regulated EMT, and several EMT-regulator mRNAs are translated by a cap-independent mechanism when eIF3e levels are reduced. Stable shRNA knockdown, TGFβ ELISA, TGFβ inhibitor rescue, polysomal mRNA analysis for cap-independent translation Molecular cancer research Medium 26056130
2016 INT6/EIF3E promotes homologous recombination-mediated DSB repair by facilitating RNF8 recruitment to DSBs and K63-linked polyubiquitin chain formation; INT6 silencing impairs RNF8 accumulation (but not RNF168 or 53BP1) at DSBs, and reduces BRCA1, BRCA2, and RAD51 recruitment, with MDC1 localization also altered, consistent with defective ATM retention reported previously. RNAi silencing, immunofluorescence of repair factors at laser-induced DSBs, ubiquitin chain analysis, HR repair assay Cancer research High 27550454
2021 eIF3e depletion in breast cancer cells causes reduced PARP1 protein synthesis due to weakened translation of PARP1 mRNA, decreased poly(ADP-ribosyl)ation, and aberrant mTORC1 activation, collectively inducing cellular senescence with a pro-inflammatory secretory phenotype. siRNA knockdown, polysome profiling of PARP1 mRNA, western blotting, mTORC1 activity assay, senescence assays (SA-β-gal, SASP markers) Oncotarget Medium 33868586
2022 INT6/eIF3e negatively regulates HIF2α protein stability in an oxygen-independent manner; INT6 knockdown leads to HIF2α accumulation, which binds TWIST1 and together represses the E-cadherin gene promoter, driving EMT in lung carcinoma A549 cells. siRNA knockdown, western blotting for HIF2α, co-immunoprecipitation (HIF2α–TWIST1), chromatin immunoprecipitation at E-cadherin promoter, EMT marker analysis Genes to cells Medium 36116043
2024 TRIM35 E3 ubiquitin ligase promotes ubiquitination and degradation of EIF3E; TRIM35 overexpression inhibits endometrial cancer cell proliferation via CDK4/Cyclin D1 pathway suppression, and EIF3E overexpression reverses TRIM35-mediated inhibition, establishing EIF3E as a TRIM35 substrate. Co-immunoprecipitation, ubiquitination assay, lentiviral overexpression/knockdown, proliferation assays, CDK4/Cyclin D1 western blotting Cellular signalling Medium 41429342
2025 ALDH2 physically interacts with eIF3E within the eIF3 complex and prevents eIF3E–eIF4G1–mRNA assembly; the ALDH2*2 loss-of-function variant disrupts this interaction, releasing eIF3E to assemble an eIF3E–eIF4G1–mRNA ternary complex that drives selective translation of mRNAs containing a GAGGACR motif (including TFRC, ACSL4, UAP1), promoting ferroptosis in cardiomyocytes during myocardial infarction. Co-immunoprecipitation (ALDH2–eIF3E), cardiomyocyte-specific AAV knockdown of eIF3E in mice, lipidomics, MS-based proteomics, motif analysis of selectively translated mRNAs Circulation High 41111418
2025 eIF3e (together with eIF3d) mediates a selective translational response to acute hypoxia, controlling HIF1α accumulation and cellular invasion; small molecules targeting eIF3e specifically reduce this hypoxia-induced translational program and also suppress ER stress-dependent translation. Ribosome profiling, siRNA knockdown of eIF3e/eIF3d, small-molecule eIF3e inhibitor characterization, HIF1α protein quantification, invasion assays Cell reports Medium 41364558
2024 eIF3e has an RNA-binding function independent of its canonical protein synthesis activity; in t(4;14) myeloma, REIIBP-upregulated eIF3e directly binds the 3'UTR of TLR7 mRNA to upregulate TLR7, demonstrating a non-canonical role of eIF3e as an RNA-binding regulator. RNA immunoprecipitation / direct binding to 3'UTR, REIIBP knockdown/overexpression, TLR7 mRNA and protein quantification Haematologica Medium 38124661
2026 Conditional deletion of Eif3e in B cells (Cγ1Cre) causes B cell hyperactivation, impaired proliferation/survival/differentiation, upregulation of CD80, and activation of CD4+ T cells into IL-4-producing TFH-like cells that in turn activate bystander Eif3e-sufficient B cells, establishing a feedforward loop that drives malignant lymphocyte transformation; this identifies eIF3e as a translational checkpoint maintaining immune tolerance. Conditional knockout mouse (Cγ1Cre-Eif3e), flow cytometry, B/T cell co-culture, IL-4 quantification, lymphoproliferation/transformation assessment The Journal of experimental medicine Medium 42233886

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Translation initiation factor eIF4G-1 binds to eIF3 through the eIF3e subunit. The Journal of biological chemistry 144 16766523
1997 The translation initiation factor eIF3-p48 subunit is encoded by int-6, a site of frequent integration by the mouse mammary tumor virus genome. The Journal of biological chemistry 130 9295280
2005 PCI proteins eIF3e and eIF3m define distinct translation initiation factor 3 complexes. BMC biology 121 15904532
2007 The tumor suppressor eIF3e mediates calcium-dependent internalization of the L-type calcium channel CaV1.2. Neuron 73 17698014
2002 Malignant transformation by the eukaryotic translation initiation factor 3 subunit p48 (eIF3e). FEBS letters 71 11904180
2001 Reduced expression of INT-6/eIF3-p48 in human tumors. International journal of oncology 71 11115556
2012 The human T-lymphotropic virus type 1 tax protein inhibits nonsense-mediated mRNA decay by interacting with INT6/EIF3E and UPF1. Journal of virology 70 22553336
2010 An oncogenic role of eIF3e/INT6 in human breast cancer. Oncogene 53 20453879
2007 Human INT6/eIF3e is required for nonsense-mediated mRNA decay. EMBO reports 49 17468741
2008 Int6/eIF3e promotes general translation and Atf1 abundance to modulate Sty1 MAPK-dependent stress response in fission yeast. The Journal of biological chemistry 39 18502752
2010 Int6/eIF3e silencing promotes functional blood vessel outgrowth and enhances wound healing by upregulating hypoxia-induced factor 2alpha expression. Circulation 36 20713899
2001 Moe1 and spInt6, the fission yeast homologues of mammalian translation initiation factor 3 subunits p66 (eIF3d) and p48 (eIF3e), respectively, are required for stable association of eIF3 subunits. The Journal of biological chemistry 36 11705997
2014 Int6/eIF3e is essential for proliferation and survival of human glioblastoma cells. International journal of molecular sciences 35 24481065
2001 Saccharomyces cerevisiae protein Pci8p and human protein eIF3e/Int-6 interact with the eIF3 core complex by binding to cognate eIF3b subunits. The Journal of biological chemistry 34 11457827
2012 Decreased eIF3e/Int6 expression causes epithelial-to-mesenchymal transition in breast epithelial cells. Oncogene 32 22907435
2007 Expression of truncated Int6/eIF3e in mammary alveolar epithelium leads to persistent hyperplasia and tumorigenesis. Breast cancer research : BCR 26 17626637
2011 Expression of truncated eukaryotic initiation factor 3e (eIF3e) resulting from integration of mouse mammary tumor virus (MMTV) causes a shift from cap-dependent to cap-independent translation. The Journal of biological chemistry 24 21737453
2010 The roles of stress-activated Sty1 and Gcn2 kinases and of the protooncoprotein homologue Int6/eIF3e in responses to endogenous oxidative stress during histidine starvation. Journal of molecular biology 24 20875427
2004 Cell cycle-related variation in subcellular localization of eIF3e/INT6 in human fibroblasts. Cell proliferation 23 15030549
2003 Protein homeostasis: a degrading role for Int6/eIF3e. Current biology : CB 22 12699646
2015 Decreased eIF3e Expression Can Mediate Epithelial-to-Mesenchymal Transition through Activation of the TGFβ Signaling Pathway. Molecular cancer research : MCR 20 26056130
2007 Expression of EIF3-p48/INT6, TID1 and Patched in cancer, a profiling of multiple tumor types and correlation of expression. Journal of biomedical science 19 17385060
2012 INT6/EIF3E interacts with ATM and is required for proper execution of the DNA damage response in human cells. Cancer research 15 22508697
2017 The Bad, the Good and eIF3e/INT6. Frontiers in bioscience (Landmark edition) 14 27814599
2021 MiR-335-3p inhibits cell proliferation and induces cell cycle arrest and apoptosis in acute myeloid leukemia by targeting EIF3E. Bioscience, biotechnology, and biochemistry 10 34191006
2018 The Possible Role of Eukaryotic Translation Initiation Factor 3 Subunit e (eIF3e) in the Epithelial-Mesenchymal Transition in Adenomyosis. Reproductive sciences (Thousand Oaks, Calif.) 9 29871559
2018 Int6/eIF3e Silencing Promotes Placenta Angiogenesis in a Rat Model of Pre-eclampsia. Scientific reports 9 29895936
2013 Int6/eIF3e silenced HIF2α stabilization enhances migration and tube formation of HUVECs via IL-6 and IL-8 signaling. Cytokine 8 23478175
2021 Decreased expression of the translation factor eIF3e induces senescence in breast cancer cells via suppression of PARP1 and activation of mTORC1. Oncotarget 7 33868586
2016 INT6/EIF3E Controls the RNF8-Dependent Ubiquitylation Pathway and Facilitates DNA Double-Strand Break Repair in Human Cells. Cancer research 7 27550454
2025 ALDH2/eIF3E Interaction Modulates Protein Translation Critical for Cardiomyocyte Ferroptosis in Acute Myocardial Ischemia Injury. Circulation 6 41111418
2024 Epigenetic dysregulation of eukaryotic initiation factor 3 subunit E (eIF3E) by lysine methyltransferase REIIBP confers a pro-inflammatory phenotype in t(4;14) myeloma. Haematologica 4 38124661
2025 Dynamic eIF3-S6 Phase Separation Switch Instructed by m6A Modification Drives the Molting of Locusts. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2 40720757
2025 eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by small molecules. Cell reports 2 41364558
2022 INT6/eIF3e represses E-cadherin expression through HIF2α in lung carcinoma A549 cells. Genes to cells : devoted to molecular & cellular mechanisms 2 36116043
2015 Silencing of eIF3e promotes blood perfusion recovery after limb ischemia through stabilization of hypoxia-inducible factor 2α activity. Journal of vascular surgery 2 25758454
2024 Identification of Rare EIF3E::RSPO2 Fusion in Recurrent and Aggressive Urachal Adenocarcinoma. Genes, chromosomes & cancer 1 38884183
2026 eIF3e-mediated translational checkpoint maintains immune tolerance and prevents lymphoid malignancy. The Journal of experimental medicine 0 42233886
2025 eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by novel small molecules. bioRxiv : the preprint server for biology 0 40501575
2025 TRIM35 inhibits endometrial cancer progression via ubiquitination and degradation of EIF3E. Cellular signalling 0 41429342

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