eIF4E (Phospho_Ser209) Antibody
- Known as:
- eIF4E (Phospho_Ser209) Antibody
- Catalog number:
- E011233-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- eIF4E (Phospho_Ser209) Antibody
Related genes to: eIF4E (Phospho_Ser209) 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 (Phospho_Ser209) Antibody
Related articles to: eIF4E (Phospho_Ser209) Antibody
- Aging is associated with declining mitochondrial function and translational regulation-processes modulated by interventions such as dietary restriction (DR) and cold-induced longevity (CHIL). Both DR and CHIL inhibit global protein synthesis but selectively enhance translation of proteins that support mitochondrial efficiency, stress resistance, and lifespan extension. These translational shifts are mediated, at least in part, by the 4E-BP/eIF4E pathway, which regulates translation according to mRNA 5'-untranslated region (5'-UTR) length and structure. To identify compounds that mimic the beneficial effects of DR/CHIL, we developed a cell-based phenotypic screen that reports on mRNA translation as a function of 5'-UTR length. A pilot screen identified compounds that preferentially increased the expression of mRNAs with short 5'-UTRs relative to those with long 5'-UTRs, and these hits were enriched for known lifespan-extending agents, such as curcumin and rapamycin. Among the novel candidates, fluspirilene significantly extended life in both Drosophila melanogaster and Caenorhabditis elegans, and mitigated age-related locomotor decline in female flies. Fluspirilene-mediated longevity in C. elegans required the DAF-16/FOXO and HLH-30/TFEB transcription factors and the autophagy gene, atg-18. Fluspirilene failed to extend lifespan in two other Caenorhabditis species, as well as in flies maintained on a high-yeast diet, indicating that its pro-longevity effects are constrained by evolutionary divergence and nutrient status. Together, our findings identify fluspirilene as a novel modulator of translation that extends life and preserves healthspan via an autophagy-dependent mechanism and support the promise of drug discovery efforts that modulate translation state as a therapeutic strategy for healthy aging. - Source: PubMed
Publication date: 2026/06/19
Wu BinbinWang Li-JieGodbole Adwait AHan Ji HeonKeebaugh Erin SChavez GisselleSedore Christine AColeman-Hulbert Anna LJohnson ErikPhillips Patrick CLithgow Gordon JDriscoll MonicaGill Matthew SJa William W - Q. Jiang , F. Li , K. Shi , P. Wu , J. An , Y. Yang and C. Xu , "ATF4 Activation by the p38MAPK-eIF4E Axis Mediates Apoptosis and Autophagy Induced by Selenite in Jurkat Cells," FEBS Letters 587, no. 15 (2013): 2420-2429, https://doi.org/10.1016/j.febslet.2013.06.011. The above article, published online on 19 June 2013 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Michael Brunner; the Federation of European Biochemical Societies; and John Wiley & Sons Ltd. The retraction has been agreed upon following concerns raised by a third party. An investigation identified several instances in which elements appear to be duplicated across different figures, including between Figures 1B and 3F, 2C and 5F, 5F and 6A, and 3E and 5E. Additional duplications were identified within Figures 1C and 5B. Further duplications were observed involving elements from Figures 1A, 1C, 3E, and 6D of this article and figures published in a later article elsewhere by some of the same authors. The authors acknowledged some of the duplications and indicated that these arose during figure preparation. Due to the time that has elapsed since publication, the original data are no longer available. The editors consider the results and conclusions of this article to be unreliable. The authors did not respond to our notice of retraction. - Source: PubMed
Publication date: 2026/06/17
- Cancer proteogenomics has revealed that RNA abundance often poorly predicts protein output, highlighting translation as a central determinant of malignant identity. In this issue of JCI, Mishra et al. showed that pharmacologic inhibition of eIF4E cap binding selectively rewired the prostate cancer translatome, suppressing basal keratin translation while promoting luminal features and renewed sensitivity to hormone therapy. More broadly, the study illustrates how tumors exploit selective translation to maintain lineage plasticity, survival, and therapeutic resistance. Targeting translational dependencies may therefore offer a powerful strategy to dismantle cancer-specific proteomic programs and convert resistant cell states into druggable vulnerabilities. - Source: PubMed
Publication date: 2026/06/15
Ruggero Davide - Mutant KRAS-driven control of protein synthesis remains poorly defined. Here, we define KRAS-dependent translational programs and their acute remodeling upon KRAS inhibition. We find that mutant KRAS controls the translation of a subset of mRNAs and affects the production of proteins of the mRNA translation apparatus. Interestingly, these specific subsets of mRNAs have short, weakly folded 5'UTRs and harbor low folding energy consensus RNA sequences. We observe ribosome accumulation on selective mRNAs. Our findings clarify the indispensable role of mutant KRAS in regulating mRNA translation, setting it apart from the other previously known mechanisms that depend on mTOR and EIF4E-EIF4A signals. Our findings uncover a mechanism by which mutant KRAS selectively uncouples the translation of mRNAs for protein synthetic machinery from the broader mRNA pool, redefining our understanding of the oncogenic regulation of mRNA translation in cancer. - Source: PubMed
Publication date: 2026/06/11
Shrivastava AnkitaPederson Eric NelsNguyen Trang UyenChuen JackyMohan PrathibhaPande ShivangiToribio Ana RuizLecomte NicolasMelchor JerryMcAuliffe John CGrandgenett Paul MRajasekhar Vinagolu KNishikawa KailaKnörlein AnnaDavid YaelWillis Ian MIacobuzio-Donahue Christine AOuyang ZhengqingSingh Kamini - The study aimed to evaluate the effects of full-fat rice bran (FFRB; Tainung No. 81, Taiwan) at various doses on insulin resistance, muscle atrophy, and gut microbiota composition in middle-aged ovariectomized (OVX) mice fed a high-fat diet (HFD), using young sham-operated mice as a life-stage reference group. Thirty-six female ICR mice were assigned to six groups, including OVX mice fed HFD with or without 5%, 10%, or 20% FFRB. Compared with HFD-fed OVX controls, 20% FFRB reduced body weight gain by 43%, decreased visceral fat mass, and improved insulin resistance (homeostasis model assessment of insulin resistance, HOMA-IR reduced by 65%, = 0.001). FFRB attenuated the decline in relative grip strength (forelimb, = 0.013; four-limb, < 0.001), and upregulated muscle protein synthesis genes, including insulin receptor substrate 1 (IRS-1), mammalian target of rapamycin (mTOR), eukaryotic translation initiation factor 4E binding protein 1 (eIF-4EBP1), while downregulating forkhead box protein O1 (FOXO1), muscle RING-finger protein-1 (MuRF-1), and interleukin (IL)-6. FFRB was also associated with higher fecal acetate levels ( < 0.001), upregulated colonic tight junction genes (occludin and zonula occludens (ZO)-1), and greater relative abundance of . Correlation analyses revealed positive associations between short-chain fatty acids (SCFAs) and muscle strength, muscle anabolic markers, genus , and . Dietary inclusion of FFRB was associated with favorable metabolic and muscle-related parameters in HFD-fed middle-aged OVX mice, with potential involvement of gut microbiota and SCFA alterations. - Source: PubMed
Publication date: 2026/05/30
Loe Pei YuOhsaki YusukeYang Suh-ChingShirakawa HitoshiChiu Wan-Chun