Ask about this productRelated genes to: Eif4e antibody
- Gene:
- EIF4E NIH gene
- Name:
- eukaryotic translation initiation factor 4E
- Previous symbol:
- EIF4EL1, EIF4F
- Synonyms:
- EIF4E1
- Chromosome:
- 4q23
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-09
- Date modifiied:
- 2015-08-25
Related products to: Eif4e antibody
Related articles to: Eif4e antibody
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder and a growing public health concern. Its core pathological features include cerebral amyloid-β deposition and tau aggregation. mRNA translation is a tightly regulated process essential for gene expression and protein synthesis. It plays critical roles in neural development, synaptogenesis, and synaptic plasticity. In recent years, dysregulated translational control has been recognized as an important pathogenic mechanism in several neurological diseases, including AD. This review provides an integrated overview of the biological basis and mechanisms of dysregulated mRNA translation in AD, including translation initiation and elongation, local synaptic translation, abnormalities in RNA-binding proteins and stress granules, tRNA dysregulation, and the effects of AD-related genetic factors on translational control. Beyond the classic mechanisms of protein aggregation, the onset and progression of AD are also accompanied by abnormal translational regulation, involving initiation, elongation, and local synaptic translation. A major feature of these abnormalities is the coexistence of suppressed global protein synthesis and selectively enhanced translation of certain disease-related mRNAs, involving the integrated stress response, eIF2α/eIF4E signaling, eEF2K/eEF2 pathway, and RNA-binding protein dysfunction. Translational dysregulation provides a new perspective for understanding the molecular pathology of AD and has prompted the exploration of interventions targeting key nodes in translational control. Strategies targeting the integrated stress response, cap-dependent translation initiation, eEF2K, and tau-RNA-binding protein interactions have shown potential to improve synaptic function and cognitive phenotypes in animal models, although their safety and clinical translatability require further evaluation. This review provides an up-to-date reference for understanding translation-centered mechanisms in AD and evaluating emerging therapeutic strategies targeting translational control. - Source: PubMed
Publication date: 2026/10/02
Li LingDai FangyuLiu HaipengHe SongbinZhang XiongTao Qing-Qing - Cancer progression is driven by coordinated dysregulation of signaling and gene-expression programs that sustain multiple hallmarks of malignancy. Eukaryotic initiation factor 4E (eIF4E) has emerged as an important determinant of this translational reprogramming by preferentially enhancing the synthesis of proteins that support oncogenic phenotypes. This review critically examines the mechanistic evidence linking eIF4E-dependent translation to major cancer hallmarks, including sustained proliferative signaling, evasion of apoptosis, tumor-promoting inflammation, angiogenesis, invasion, and metastasis. We discuss how dysregulated eIF4E activity, driven in part by the PI3K/AKT/mTOR and MAPK/MNK pathways, promotes selective translation of oncogenic, survival, stress-response, hypoxia-, and epithelial-mesenchymal transition-associated factors. We further examine evidence implicating eIF4E in the regulation of p53- and telomerase reverse transcriptase (TERT)-dependent pathways, highlighting potential links to genomic instability and replicative immortality. Finally, we evaluate pharmacological strategies targeting eIF4E and discuss the opportunities and challenges of exploiting eIF4E-dependent translational and metabolic vulnerabilities for cancer therapy. Collectively, the evidence supports eIF4E as a therapeutically relevant translational regulator whose functional activity, rather than expression alone, may help define tumor dependencies and inform mechanism-based therapeutic strategies. - Source: PubMed
Publication date: 2026/10/02
Udobi Magdalene EnoEffiong Paul EtimRoy SumonOkafor Chibuike EmmanuelSchober Joseph MAun Lionel In LianPatel Bhargav A - Proviral integration site for Moloney murine leukemia virus (PIM) kinase family (PIM1, PIM2, and PIM3) comprises constitutively active serine/threonine kinases that function as proto-oncogenic and immune-inflammatory signaling nodes. In cancer, PIM kinases promote tumor growth, therapeutic resistance, and immune microenvironment remodeling by phosphorylating substrates such as BCL2-associated agonist of cell death (BAD), Myc proto-oncogene protein (c-MYC), proline-rich AKT substrate of 40 kDa (PRAS40), and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1)/eukaryotic translation initiation factor 4B (eIF4B), while integrating with Janus kinase/signal transducer and activator of transcription (JAK/STAT), phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR), nuclear factor kappa B (NF-κB), and NOD-like receptor family pyrin domain-containing 3 (NLRP3) signaling. In immune-inflammatory disorders, particularly through PIM1-dependent macrophage and T-cell regulation, these kinases amplify inflammatory signaling and contribute to pathological tissue remodeling. This review systematically summarizes the PIM kinase structural features, isoform-specific biology, signaling networks, disease-context dependency, inhibitor chemotypes, clinical development, and translational limitations of PIM-targeted therapy. We emphasize medicinal-chemistry strategies designed to exploit PIM dependency, including isoform-biased design, and emerging degrader-based approaches. PIM inhibitors have advanced from preclinical validation to clinical trials, but their clinical translation remains challenged by modest monotherapy activity, off-target toxicities, lack of validated predictive biomarkers, and paradoxical inhibitor-induced PIM stabilization. Therefore, future success will require the integration of rational combination therapies targeting PI3K/AKT/mTOR, JAK, proteasome, and immune-checkpoint pathways; structure-guided next-generation modalities, including isoform-selective inhibitors and targeted protein degraders; and biomarker-driven patient stratification to effectively translate PIM-targeted therapies into clinical practice. - Source: PubMed
Publication date: 2026/09/25
Li QingyanQiu QiangDing LinGou LipingYang TaoYang LinyuChen Lijuan - Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by deficits in social communication and interaction, and restricted interests or repetitive behaviors. ASD is approximately four times more prevalent in males than in females. In this study, we investigated whether sex hormones or sex chromosomes underlie the male bias in ASD susceptibility. - Source: PubMed
Publication date: 2026/09/07
Niu ChangranAn Juan JiMasterson Hannah VXu Baoji - Group 1 metabotropic glutamate receptors (Gp1 mGluRs) are critical effectors in behavior. Abnormal Gp1 mGluR signaling is frequently observed in neurodevelopmental and cognitive disorders. It is established that activation of Gp1 mGluR elicits translation-dependent neuronal plasticity mechanisms, such as long-term synaptic depression (LTD). However, whether and how transcription is involved is not clear. In this study, we study a cellular stress associated transcription factor, activation transcription factor 4 (ATF4). We first employed RNA sequencing and revealed that knocking down ATF4 using ATF4 heterozygous mice upregulates or downregulates multiple genes with known functions in translational control or synaptic plasticity in a sex-dependent manner. When searching for a crosstalk between ATF4 and known synaptic plasticity mechanisms, we found that activation of Gp1 mGluR promotes the expression and nuclear distribution of ATF4. Using ATF4 heterozygous mice, we further confirmed that ATF4 is required for Gp1 mGluR-induced activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and phosphorylation of eukaryotic translation initiation factor 4E (eIF4E), de novo translation and hippocampal LTD at Schaffer-collateral synapses. When assessing animal behavior, our results indicated that knocking down ATF4 impairs learning behavior and precludes mGluR-dependent reduction in repetitive behavior only in female mice. Altogether, our study suggests ATF4 as an activity-dependent transcription factor required for Gp1 mGluR-dependent translation, hippocampal LTD, and behavior. - Source: PubMed
Publication date: 2026/09/30
Wang ShiyuYook YeeunLizarazo SimonLee Kwan YoungVan Bortle KevinRhodes Justin SChristian-Hinman Catherine ATsai Nien-Pei