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
- Colorectal cancer (CRC) remains one of the leading causes of cancer-related mortality worldwide, yet the underlying mechanisms driving its progression are not fully elucidated. Long non-coding RNAs (lncRNAs) have recently emerged as key regulatory molecules in tumor biology. In this study, we identified ABHD11-AS1 as a tumor-suppressive lncRNA that is significantly downregulated in CRC tissues, its low expression is correlated with poor patient prognosis. Functional assays demonstrated that ABHD11-AS1 inhibits CRC cell proliferation, migration, and invasion, and enhances sensitivity to oxaliplatin. Mechanistically, ABHD11-AS1 directly binds to EIF4E and disrupts its phase separation, thereby suppressing the translation of USP18, a deubiquitinating enzyme that stabilises the oncogenic protein POU2F1. Reduced USP18 expression leads to increased ubiquitination and proteasomal degradation of POU2F1, ultimately inhibiting malignant progression and enhancing chemotherapy sensitivity. Collectively, our findings uncover a previously unrecognised mechanism by which ABHD11-AS1 modulates EIF4E-mediated phase separation to regulate protein homeostasis, highlighting its potential as a therapeutic target in CRC. - Source: PubMed
Publication date: 2026/04/23
Li ShizhenJiang XianjieOyang LindaXia LongzhengTan ShimingRen ZongyaoPeng QiuLin JinguanLiao QianjinZhou Yujuan - The ability to adapt to nutrient stress, such as amino acid limitation, is crucial for cell survival. The mTORC1 complex and integrated stress response (ISR) are two mechanisms that sense the availability of amino acids and regulate protein synthesis. Here, we reveal a new SIRT2-mediated pathway, downstream of the ISR, that is activated under amino acids limitation to suppress global translation. Under amino acid deprivation, SIRT2 protein level is upregulated translationally by its upstream open reading frame (uORF). SIRT2 in turn suppresses translation, which helps cells to survive amino acid limitation. We identify eukaryotic translation initiation factor 4E (eIF4E) binding protein 1 (4E-BP1), which binds to eIF4E and inhibits translation, as a substrate of SIRT2. SIRT2 deacetylates 4E-BP1 at lysine 69 and stabilizes 4E-BP1 by protecting it from proteasomal degradation, leading to suppression of global translation. Our study uncovers a role for SIRT2 in regulating translation and identifies a new regulatory mechanism of 4E-BP1 in cells. - Source: PubMed
Publication date: 2026/05/18
Zi YanlinZhao JiaqiWang MiaoHou DanCerione Richard ALin Hening - Herpes simplex virus type 2 (HSV-2) is the principal cause of genital herpes, establishes lifelong latency with recurrent mucosal lesions, and facilitates acquisition of human immunodeficiency virus type 1 (HIV-1). Because current therapy still relies largely on nucleoside analogues and resistant isolates continue to emerge, alternative antiviral strategies are needed. In this study, halofuginone (HF), a halogenated analogue of the febrifugine scaffold, inhibited both wild-type and acyclovir-resistant HSV-2 in cultured cells at nanomolar concentrations. In a murine genital challenge model, topical administration before viral exposure reduced viral burden and alleviated local inflammatory responses. Pre-exposure experiments further showed that HF decreased the infectivity of extracellular HSV-2 particles and was associated with virion structural damage, whereas docking analysis suggested a possible interaction with glycoprotein D (gD). In parallel, partial reversal by L-proline supported a host-cell component linked to inhibition of the prolyl-tRNA synthetase (ProRS) domain of glutamyl-prolyl-tRNA synthetase (EPRS). HF also suppressed HSV-2-induced activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) axis and the nuclear factor kappa B (NF-κB) pathway. Beyond HSV-2, HF remained active against herpes simplex virus type 1 (HSV-1) and C-C chemokine receptor type 5 (CCR5)-tropic HIV-1 and retained antiviral activity in an HSV-2/HIV-1 co-infection model. Overall, the data support a two-component antiviral effect of HF, involving extracellular impairment of viral particles together with intracellular host-directed restriction, and warrant further evaluation of HF as a topical prevention-oriented candidate against HSV-2. - Source: PubMed
Publication date: 2026/05/14
Pan ZhizhiChen ZhuoHuang XiaolinLin YueningLi LinLiu ShuwenTan Suiyi - Ageing leads to changes in body composition, including increased adiposity and reduced skeletal muscle mass and force. The alterations in ageing skeletal muscle result from impaired proteostasis driven by factors such as chronic inflammation, hormonal changes and reduced nutrient absorption. Those age-related changes in body composition and skeletal muscle compromise mobility and increase the risk of falls, fractures and metabolic disorders. Tauroursodeoxycholic acid (TUDCA), a bile acid with known benefits in chronic diseases, has been shown by our group to improve cognition and metabolic homeostasis in ageing and Alzheimer's disease mouse models. Interestingly, in previous studies, TUDCA treatment was also associated with increased skeletal muscle mass in ageing mice, leading us to hypothesize that TUDCA could target skeletal muscle to reduce age-related muscle loss. To explore this, we treated 18-month-old C57BL/6 mice with TUDCA or vehicle for 20 days, using 3-month-old mice as a young control group. We demonstrate that TUDCA treatment decreases body weight while increasing skeletal muscle mass, restores muscle fibre size and preserves functional integrity. Additionally, TUDCA enhances skeletal muscle insulin sensitivity through increased AKT activation and reduces tissue inflammation. Such improvements collectively support the restoration of skeletal muscle proteostasis, as indicated by increased protein synthesis and phosphorylation of key anabolic signalling pathways, including ribosomal protein S6 kinase beta-1 (P70S6K) and eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1). These findings contribute to a better understanding of TUDCA's actions on skeletal muscles of ageing mice and highlight its role as a promising strategy against age-related muscle loss. KEY POINTS: Tauroursodeoxycholic acid (TUDCA) treatment attenuates skeletal muscle loss in ageing mice. TUDCA improves skeletal muscle insulin sensitivity and restores AKT signalling. TUDCA exerts an anti-inflammatory effect in skeletal muscle of ageing mice. TUDCA emerges as a potential therapy for age-related skeletal muscle loss. - Source: PubMed
Publication date: 2026/05/15
Carvalho Marina SBarssotti LeticiaSantos Lohanna M B DosRosa Lucas R OGomes-Marcondes Maria Cristina CCarneiro Everardo MBarbosa Helena C LZangerolamo Lucas - Eukaryotic translation initiation factor 4E (eIF4E) plays an essential role in driving the translation of mRNAs that promote cell proliferation. Its activity is regulated through phosphorylation at Ser209 by MNK1/2 kinases, which are downstream effectors of mitogen-activated protein kinase signaling. Elevated eIF4E phosphorylation drives malignant progression in multiple cancers, including glioblastoma, where it promotes translation of key oncoproteins responsible for tumor growth and therapy resistance. Here, we report the development and application of a direct-to-biology (D2B) platform to rapidly optimize new MNK inhibitors for cellular inhibition. This approach combines plate-based library synthesis with an in-cell Western assay to efficiently generate structure-activity relationship (SAR) data and new compounds with potent cellular inhibition. Using this platform, we synthesized and tested >150 new analogs directly in cells, identifying inhibitors with IC values as low as 23 nM in LN229 cells. This work establishes a D2B approach as an effective strategy for efficient kinase inhibitor optimization. - Source: PubMed
Publication date: 2026/05/13
Vagadia Purav PMao YingyuEckerdt FrankZhu Joshua LPlatanias Leonidas CSchiltz Gary E