Ask about this productRelated genes to: 4E-BP1 antibody
- Gene:
- EIF4EBP1P1 NIH gene
- Name:
- eukaryotic translation initiation factor 4E binding protein 1 pseudogene 1
- Previous symbol:
- EIF4EBP1P
- Synonyms:
- -
- Chromosome:
- 14q11.2
- Locus Type:
- pseudogene
- Date approved:
- 2003-01-13
- Date modifiied:
- 2014-11-28
Related products to: 4E-BP1 antibody
Related articles to: 4E-BP1 antibody
- Traumatic brain injury (TBI) is a leading cause of mortality and long-term neurological disability, while effective pharmacological therapies for its neurobehavioral consequences remain limited. This systematic review evaluates the therapeutic potential of Ginkgo biloba (GB), particularly the standardized extract EGb 761, in TBI management. A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science up to February 2026. Sixty-five studies met the inclusion criteria, including 42 in vivo experimental studies and 23 clinical trials examining neuroprotective, cognitive, behavioral, or functional outcomes following GB administration. Preclinical evidence consistently demonstrates that Ginkgo biloba (GB) exerts neuroprotective effects through attenuation of oxidative stress, as evidenced by increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, alongside reduced malondialdehyde (MDA) levels. These effects are accompanied by modulation of the Slc7a11-Eif4ebp1 signaling axis, suppression of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α, and regulation of key molecular pathways. Specifically, GB inhibits JAK/STAT and TXNIP/NLRP3 signaling while activating PI3K/AKT-associated pathways and autophagy. Clinical studies indicate potential improvements in cognitive and functional outcomes. However, adverse events, particularly bleeding, have been reported, especially when GB is co-administered with anticoagulants or nonsteroidal anti-inflammatory drugs. This underscores the importance of careful patient monitoring. The current evidence supports the promising neuroprotective potential of GB in traumatic brain injury. Nevertheless, clinical data remain insufficient to justify routine therapeutic use. Large-scale, well-designed, randomized controlled trials are necessary to confirm efficacy, optimize dosing regimens, and establish long-term safety profiles. - Source: PubMed
Nazeam Jilan AMahmoud OmniaSaad AmiraHassan AmiraSaleh OmniaAlaaeldein AmiraAli EtharEzzat AndrewBahaa EhdaaMgahd AndrewEl-Shazly MohamedElgayed Sabah H - Colorectal cancer (CRC) persists as a significant public health burden due to its high morbidity and mortality rates worldwide, yet the molecular events that govern its initiation and progression remain incompletely understood. We recently conducted microRNA (miRNA) profiling and identified multiple dysregulated miRNAs in CRC compared to adjacent normal tissue. Among those, miR-138-5p emerged as a potential tumor suppressor due to its marked downregulation in CRC tissue; however, the stage-specific expression of this miRNA during CRC progression and underlying molecular mechanisms remains to be unraveled. In this study, we performed differential expression profiling of healthy colon, adenomatous polyp (AP), and CRC tissues based on public datasets, revealing significant downregulation of miR-138-5p in CRC compared to controls, but not during the AP stage, suggesting a role in later stages of malignant progression. Forced expression of miR-138-5p in HCT116 and HT-29 CRC models suppressed clonogenic survival, proliferation, and migration while inducing cell death. Additionally, miR-138-5p significantly inhibited tumor formation under three-dimensional culture settings, reinforcing its tumor-suppressive function in a physiologically relevant context. Transcriptomic profiling of miR-138-5p-overexpressing CRC models revealed widespread changes in the pathways related to zinc ion binding, cilium morphogenesis, smoothened signaling, and nuclear transport. Integrated computational and experimental analyses identified 41 potential gene targets, among which , and were validated as potential miR-138-5p-regulated genes. Collectively, these findings establish miR-138-5p as a stage-specific tumor suppressor in CRC, acting through coordinated regulation of oncogenic networks across multiple pathways. Downregulation of miR-138-5p appears to be a late oncogenic event, conferring proliferative, survival, and invasive advantages to tumor cells. Restoration of miR-138-5p or therapeutic targeting of its downstream effectors may represent promising avenues for CRC therapeutic intervention. - Source: PubMed
Publication date: 2026/04/09
Shaath HibahVishnubalaji RadhakrishnanAlajez Nehad M - Emerging evidence reveals the pivotal involvement of mitochondrial metabolic dysregulation in glioblastoma (GBM) pathogenesis, considering mitochondrial metabolism as a potential therapeutic target. Nebivolol, a third-generation β-adrenergic receptor antagonist clinically employed in cardiovascular diseases, has recently exhibited notable anti-neoplastic properties. Nevertheless, its therapeutic efficacy and mechanistic underpinnings in GBM remain largely unexplored. In this investigation, we comprehensively assessed the impact of nebivolol on GBM cellular proliferation and elucidated its molecular mechanisms. Our findings revealed that nebivolol markedly suppressed the proliferation and clonogenic abilities of multiple GBM cell lines, concomitant with cell cycle arrest and apoptotic induction. Mechanistically, nebivolol impaired mitochondrial respiratory chain complex I activity, diminished adenosine triphosphate (ATP) synthesis, and augmented ROS production, collectively precipitating neoplastic cell apoptosis. Furthermore, nebivolol attenuated AKT/mTOR/4EBP1 signaling cascade activation, thereby impeding GBM malignant proliferation. In vivo studies corroborated these observations, demonstrating that nebivolol administration significantly attenuated orthotopic GBM xenograft progression and extended survival in tumor-bearing murine models. This study delineates a novel dual mechanism whereby nebivolol exerts anti-GBM effects through concurrent modulation of mitochondrial bioenergetics and AKT/mTOR/4EBP1 signaling transduction. These results provide robust preclinical evidence supporting nebivolol's clinical repurposing for GBM therapy. - Source: PubMed
Publication date: 2026/04/24
Zhou LingniChe HongyuJiang HongyanYin LuxinJiang YongangZhang YuhuiLiang HaoranYu RutongZhang XuLiu Xuejiao - Exposure to perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) has been associated with the development of various malignant tumors. However, their roles and molecular mechanisms in glioblastoma (GBM) are still unclear. This study combined network toxicology, machine learning, immune infiltration analysis, single-cell RNA sequencing (scRNA-seq), molecular docking, Mendelian randomization (MR), and molecular dynamics (MD) simulation to explore the potential toxicological targets and mechanisms of PFOA/PFOS in GBM. Five core target genes (ANXA5, AURKA, CDK2, EIF4EBP1, and ODC1) were identified. Their predictive potential was validated using three external independent datasets, with AUC values mostly above 0.90. Gene Set Enrichment Analysis (GSEA) revealed significant enrichment of the phosphatidylinositol, ErbB, and MAPK signaling pathways. Furthermore, the expression levels of core targets exhibited strong correlations with immune cell infiltration, particularly with macrophages and NK cells. ScRNA-seq analysis revealed that the core targets were predominantly expressed in MES‑like and AC‑like malignant cells, suggesting their potential roles in regulating the functional phenotypes of GBM cell subpopulations. Molecular docking confirmed the strong binding affinity of PFOA/PFOS with five core targets. MR analysis revealed a significant association between ODC1 expression and GBM risk (OR = 2.16, 95%CI: 1.129-4.115; P = 0.0198), while MD simulation further verified the sustained binding interactions between ODC1 and PFOA/PFOS. We also proposed a novel adverse outcome pathway (AOP) framework linking PFOA/PFOS exposure to GBM, offering critical toxicological insights. Overall, these findings provide valuable evidence for the potential toxicological impact of PFOA/PFOS on GBM, highlighting the necessity for further mechanistic investigations. - Source: PubMed
Publication date: 2026/04/21
Wang JingXu QingqinLuo YongxinZhang ZhongfuLu Jianwei - Cardiomyocytes depend on local translation for growth and can undergo directed growth in length or width in response to different stimuli. Protein synthesis is augmented during concentric hypertrophy, which leads to thickening of the heart muscle by increasing cardiomyocyte width. Protein synthesis is controlled at the translation initiation step, when ribosome loading onto transcripts is regulated by the sequential phosphorylation of the eukaryotic initiation factor 4E-binding protein 1 (4EBP1). Here, we identified a mode of 4EBP1 phosphorylation that was associated with concentric hypertrophy in cultured cardiomyocytes and mouse hearts. Whereas canonical phosphorylation of 4EBP1 by mTORC1 regulates global protein synthesis rates, mTORC1- and nuclear ERK-dependent phosphorylation of 4EBP1 was specifically activated during concentric but not eccentric hypertrophy. Nuclear ERK-dependent phosphorylation of 4EBP1 at Ser was necessary and sufficient to relocalize translation initiation sites closer to the nuclei. ERK activation drove redistribution of ribosomes and nascent translation toward the center of the cardiomyocyte without altering global mRNA distribution, leading to spatially enriched deposition of new sarcomeric protein in the cardiomyocyte interior. Together, these findings demonstrate that global protein synthesis can be spatially regulated by the activation of different kinases in distinct subcellular compartments and identify a mechanism that drives concentric hypertrophy. - Source: PubMed
Publication date: 2026/04/21
Uchida KeitaScarborough Emily APruzinsky ElizabethStone Kathlyene RHartman HaliKelly Daniel PEdwards Jonathan JKehat IzhakProsser Benjamin L