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
- The present study aimed to explore the difference and its underlying molecular mechanism of in ovo feeding (IOF) with Codonopsis pilosula polysaccharides (CPPS) on skeletal muscle in ducks. A total of 120 fertile eggs were randomly distributed into two treatment groups, with 6 replicates per group and 10 eggs per replicate. IOF was performed at incubation day 13 (I13). The control group was injected with 0.2 mL 0.75% sterile saline, while the CPPS group received 0.2 mL CPPS solution at a dose of 3 mg per egg. Breast muscle and leg muscle tissue samples were collected at I24 for multi-omics (transcriptomics, metabolomics and proteomics) analyses. In breast muscle, a total of 1301 differentially expressed genes (DEGs) were identified (497 upregulated and 804 downregulated). Genes involved in muscle development, such as creatine kinase, mitochondrial 2 (CKMT2, ENSAPLG00020008721) and G-protein signaling 4(RGS4, ENSAPLG00020014659), were significantly upregulated. For proteomics, 89 different expressed proteins (DEPs) were identified (44 upregulated and 45 downregulated), among which, Eukaryotic translation initiation factor 4E type 2 (eIF4E2, A0A8B9SQK7), myomesin 3 (A0A8B9ZBZ5), myogenic factor 6 (A0A8B9SGC1), myosin heavy chain and other myogenic-related proteins (MyHC, A0A8B9ZL15) related to muscle synthesis were markedly increased. Metabolomic analysis identified 1647 differential metabolites (DEMs), including 43 upregulated and 22 downregulated, with leucine being significantly decreased. Multi-omics integration revealed that these differential molecules were collectively enriched in the mTOR signaling pathway and glycerophospholipid metabolism pathway. These coordinated regulatory effects synergistically promoted breast muscle fiber development, enhanced energy metabolism, alleviated stress induced injury and ultimately improved skeletal muscle growth potential and meat quality. While in the leg muscles, 1195 DEGs were identified (487 upregulated and 708 downregulated), among which the expression of transcription factor 15 (TCF15, ENSAPLG00020006012), a gene associated with muscle development, was significantly upregulated. Proteomic analysis revealed 47 DEPs (15 upregulated and 32 downregulated), including phosphorus receptor protein (A0A8B9TCV3, PLN), mitofusin 1(A0A8B9TRP9, MFN1), titin(A0A8B9ZFJ8), which are closely related to muscle development and energy metabolism. Metabolomic analysis identified 1647 DEMs were identified (66 upregulated and 40 downregulated), with 5-Hydroxy-L-tryptophan (5-HTP), the precursor of serotonin (5-HT), significantly upregulated, providing substrates and energy for muscle development. Although no shared enriched pathway existed across the three omics in leg muscle, the differential molecules collectively suggest that IOF with CPPS supports energy supply for cell proliferation and creates a favorable environment for myogenesis. These findings help to elucidate the molecular mechanisms by which CPPS regulates embryonic skeletal muscle development. Moreover, the candidate genes, proteins and metabolites identified in this study may serve as valuable biomarkers and provide a potential nutritional strategy for improving meat quality traits in duck breeding. - Source: PubMed
Publication date: 2026/08/09
Liu AiRao YifuYue YongZhu JinjinWen JiyingYao BiqiongZhu YongcaiBoonanuntan SurintornYang Shenglin - Eukaryotic initiation factor 4E-binding protein 1 (EIF4EBP1/4E-BP1) is a pivotal translational regulator with context-dependent roles in breast cancer pathogenesis. Its phosphorylation status, dynamically controlled by mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK), and AMP-activated protein kinase (AMPK) signaling, dictates a dualistic function: hypophosphorylated EIF4EBP1 suppresses oncogenesis by sequestering eIF4E and inhibiting cap-dependent translation of pro-tumorigenic mRNAs (e.g., cyclin D1 and c-MYC), while hyperphosphorylation promotes tumor progression and therapeutic resistance. EIF4EBP1 amplification (8p11-p12) is correlated with endocrine resistance and poor prognosis. EIF4EBP1 modulates cell cycle checkpoints, metabolic adaptation under stress, and resistance to cyclin-dependent kinase (CDK) 4 and 6 inhibitors and rapalogs via feedback loops (e.g., SGK3/Akt reactivation). Emerging therapeutic strategies, such as ATP-competitive mTOR inhibitors, bisteric compounds, and agents targeting polyamine metabolism or upstream kinases, exploit the dynamics of EIF4EBP1 phosphorylation. As a biomarker, phosphorylated EIF4EBP1 levels predict tumor aggressiveness and treatment failure, positioning it as a critical node for precision oncology. Future research must address spatial heterogeneity and leverage multi-omics/AI-driven approaches. - Source: PubMed
Liu WeijiaHou LiliTang DandanMou HaiyuWang WeijieLiu Song-BaiLi Xiaohua - Repurposing of approved drugs offers a rapid and cost-effective strategy for the identification of new therapeutic applications, particularly for difficult-to-treat and therapy-resistant cancers. Ribavirin, which is a synthetic guanosine analog and used as an antiviral drug, has demonstrated promising anticancer activity. To that end, the literature has presented varied anticancer mechanisms of action for ribavirin. This review integrates the current mechanistic evidence and proposes a working hypothesis in which ribavirin may influence interconnected metabolic, signaling, and translational processes that collectively induce its anticancer activity. Ribavirin inhibits inosine monophosphate dehydrogenase and depletes GTP, which may influence small GTPase-dependent signaling such as Ras-driven pathways. More recently, modulation of metabolic signaling by ribavirin has been proposed through the inhibition of AMP-activated protein kinase-associated pathways. These upstream perturbations may propagate through oncogenic signaling networks and complement the suppression of eukaryotic translation initiation factor 4E-dependent mRNA export and protein synthesis. Further, ribavirin treatment indirectly influences epigenetic regulators, inflammatory mediators, and immune checkpoint pathways, contributing to broader reprogramming of tumor cell behavior. Ultimately, ribavirin's effects lead to cell cycle arrest, apoptosis, and enhanced chemosensitivity across diverse cancer types. Taken together, the available evidence supports the hypothesis that ribavirin may function as a multilevel modulator of cellular growth networks, although the mechanistic relationships among these pathways remain incompletely defined. SIGNIFICANCE STATEMENT: This review theorizes ribavirin as a systems-level anticancer agent by integrating its effects on guanine nucleotide metabolism, oncogenic signaling, and eukaryotic translation initiation factor 4E-dependent translation into a unified metabolic-signaling-translation axis. In addition, it identifies the disparities in the mechanistic literature, which may assist in designing future studies. - Source: PubMed
Publication date: 2026/08/03
Talukder Mohini AmritaOkafor Chibuike EmmanuelSchober Joseph MPatel Bhargav A - Chuju ( (Ramat.) Tzvel. cv.), a traditional Chinese medicinal herb with both medicinal and edible properties. It is widely used in tea beverages and functional foods due to its rich flavonoid and polysaccharide content. Our previous studies demonstrated that the total flavonoids of Chuju (TFCJ) alleviate cerebral ischemia-reperfusion injury (CIRI) in rats. However, the potential metabolic pathways regulated by TFCJ remain unclear, and its therapeutic targets require further investigation. This study aims to elucidate the neuroprotective mechanisms of TFCJ. LC-MS analysis identified 42 compounds within TFCJ. Animal experiments showed that TFCJ significantly reduced cerebral infarct volume, elevated SOD and GSH-Px levels, and decreased MDA levels in the brain. Non-targeted metabolomic analysis suggested that TFCJ exerts its protective effects by modulating the tricarboxylic acid (TCA) cycle, glycolysis, pentose phosphate pathway (PPP), and aspartate-glutamate metabolism. Pathway analysis revealed that the 4EBP1/eIF4E signaling pathway may mediate the protective effects of TFCJ. In conclusion, this study analyzed the main components of TFCJ and provided evidence suggesting that the 4EBP1/eIF4E signaling pathway might serve as a potential mediator of its neuroprotective effects against CIRI. These findings provide a theoretical basis for the application of TFCJ as both a functional food and a medicinal agent. - Source: PubMed
Publication date: 2026/08/27
Zhang GuangleiZhang ZongmengWang CongShi GaochengZhao MengqiWu XianxiYuan XiaoyongYu Hao - Stress-inducible phosphoprotein 1 (STIP1) is a co-chaperone involved in neuronal proteostasis and stress resilience. Although expressed in the heart, its role remains undefined. We assessed whether STIP1 deficiency impacts cardiac physiology and stress responses. STIP1 expression was analyzed in cardiac tissue from patients with heart failure. Haploinsufficient STIP1 mice (STIP1) received 7 days of isoproterenol (ISO) to induce cardiac injury, followed by proteomic, histological, and cardiomyocyte analyses. In vitro, neonatal rat cardiomyocytes (NRCMs) underwent STIP1 silencing and were evaluated using immunofluorescence, puromycin incorporation and western blotting. STIP1 levels were reduced in cardiac tissue from heart failure patients, a pattern mirrored in STIP1 mice. While STIP1 hearts developed normally, ISO exposure led to increased inflammation and fibrosis compared with wild-type. Despite elevated injury markers, STIP1 cardiomyocytes failed to undergo hypertrophy in response to ISO. Proteomic profiling identified impaired protein synthesis as the dominant signature in STIP1/ISO hearts, explaining the blunted hypertrophic response. To determine STIP1's role in cardiomyocyte hypertrophy and establish causality, we silenced STIP1 in NRCMs. Recapitulating in vivo findings, STIP1 silencing blocked ISO‑induced hypertrophy and similarly inhibited the hypertrophic responses to Ang II and phenylephrine in NRCMs. Consistent with proteomics, ISO failed to increase protein synthesis or eIF4E expression in STIP1-deficient NRCMs. STIP1 loss impairs the protein synthesis required for pathological cardiomyocyte hypertrophy, highlighting its essential role in cardiac adaptation to injury. - Source: PubMed
Publication date: 2026/08/28
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