Ask about this productRelated genes to: EIF4G1 antibody
- Gene:
- EIF4G1 NIH gene
- Name:
- eukaryotic translation initiation factor 4 gamma 1
- Previous symbol:
- EIF4G, EIF4F
- Synonyms:
- p220, PARK18
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-17
- Date modifiied:
- 2016-04-25
Related products to: EIF4G1 antibody
Related articles to: EIF4G1 antibody
- Despite significant advancements in atopic dermatitis (AD) treatment, the underlying pathogenesis remains unclear. Understanding flare and remission mechanisms is essential for understanding disease course, evaluating treatment and developing therapeutic strategies. Although biomarkers show promise for assessing disease severity, their identification, validation and clinical utility demand further research. - Source: PubMed
Publication date: 2026/04/20
Olydam Jill IsabelleLitman ThomasNijsten TamarHoof IlkaKoopmann WittePardo Luba MilenaHijnen DirkJan - Formation of a "closed-loop" mRNP, in which the 5' cap and 3' poly(A) tail are bridged by eIF4E-eIF4G-PABP interactions, has long been proposed to drive efficient translation initiation. Direct tests of this model in mammalian cells have remained elusive. Using auxin-inducible degron (AID) technology to acutely deplete eIF4G1, we find that global translation is only partially reduced and recovers without restoration of eIF4G1 levels. We identify eIF4G3 as an underappreciated contributor to basal translation that buffers translational output upon eIF4G1 loss without increased protein expression, explaining the modest defects observed in prior RNAi-based studies. Systematic replacement of eIF4G1 with defined cleavage products and interaction mutants reveals that PABP binding by eIF4G1 is dispensable for bulk translation initiation: the central caspase-3 cleavage fragment of eIF4G1 (casp3-cp), which lacks the PABP-interaction domain, fully rescues global protein synthesis, and acute depletion of both major cytoplasmic PABP paralogs primarily destabilizes mRNAs rather than impairing initiation. In contrast, the N-terminal enteroviral 2A cleavage product (2A-cp) is a potent, dominant translational repressor that requires simultaneous eIF4E and PABP engagement to form a dead-end closed-loop mRNP that sequesters initiation factors without enabling 43S recruitment. These findings reveal that the eIF4G-PABP closed-loop architecture is not required for productive initiation but can be actively co-opted for translational silencing. This explains why viral eIF4G cleavage, but not factor depletion, produces near-complete translational shutoff. The modular architecture of eIF4G enables diametrically opposing translational outcomes through selective proteolytic processing. - Source: PubMed
Publication date: 2026/04/07
Johnston RyanBrekker Mollie AKhalil NoelleGoldstein Monty EAldrich AnneGrimins Autumn OGritli SamiMarintchev AssenBlower Michael DSaeed MohsanLyons Shawn M - Non-small-cell lung cancer (NSCLC) exhibits pronounced molecular heterogeneity, and current predictive models rarely incorporate mitochondrial quality-control programs such as mitophagy. We hypothesize that an artificial intelligence model based on mitophagy-related genes (MRGs) at single-cell resolution could improve prediction of survival and immunotherapy benefit. - Source: PubMed
Publication date: 2026/03/18
Wang Ming-HaoWang YuLi Yi-TongWusiman DilinaerLu MeiZhang Cheng-YiLi Ye-XiongBi Nan - Head and neck cancer (HNC) represents the seventh most common cancer diagnosis globally, yet current treatments, including surgery, radiation, and immunotherapy, have shown limited improvement in outcomes. Drug repurposing offers a cost-effective strategy to identify new therapeutic options by leveraging existing medications with known safety profiles. Within this study, we developed the pipeline (enomic lteration-based epurposing for rugs), designed to uncover repurposing candidates for HNC using genomic and network-based approaches. : GARD integrates multi-omics data from The Cancer Genome Atlas (TCGA), including copy number variation (CNV) and somatic mutations (SOM). The cohort was stratified by human papillomavirus (HPV) status. Risk-associated genes were identified and then expanded via high-confidence protein-protein interaction (PPI) networks. Top candidate genes were filtered through comprehensive analysis of publicly available literature data in PubMed using LLMs to validate the relationship between the identified genes and HNC. The top risk genes and their network-expanded neighbors were mapped against DrugBank, and through statistical significance testing and literature validation, established significant drug-gene associations. : Significant genes associated with HNC, inferred by genomics alteration, were identified across HPV-positive and HPV-negative subgroups, such as PIK3CA, SOX2, TP53, EIF4G1, TLR7, CLDN1, PRKCI, and EPHA2. Further expansion through the PPI network identified other targetable genes such as EGFR, ERBB2, and the FGFRs. Literature-based validation efforts ensured confidence in the gene-disease association. Drug-gene mapping revealed candidates spanning those already in clinical trials for HNC (e.g., Afatinib, Cabozantinib, Dasatinib, Brigatinib, Lenvatinib, Capivasertib, and Erdafitinib) and emerging or repurposing candidates (Amuvatinib, XL765 (Voxtalisib), Golotimod, Artenimol, Quercetin, and Acetylsalicylic Acid), offering opportunities for precision repurposing. : The GARD pipeline demonstrates a genomics-driven, network-informed framework for systematic drug repurposing in HNC. HPV stratification enhances precision, literature-based validation strengthens confidence, and integrated drug mapping enables refinement of existing therapies and discovery of novel candidates for personalized treatment strategies. : The full implementation of the GARD pipeline, including preprocessing scripts, statistical analysis modules, and visualization tools, is publicly available on GitHub. - Source: PubMed
Publication date: 2026/02/26
Tanikella PradhamNenad WilliamCourtine ChristopheDai YifanDeng QingyingZou BaimingOsazuwa-Peters NosayabaSchrank Travis PWu Di - Interstitial deletions involving 3q27.1 define a distinct microdeletion syndrome characterized by prenatal-onset growth restriction, postnatal microcephaly, hypotonia, intellectual disability, and distinctive craniofacial features. While AP2M1 haploinsufficiency has been proposed as the primary driver of this phenotype, the full spectrum of dosage-sensitive genes within the locus remains unclear. Here, we report a patient with a de novo heterozygous 3q27.1 microdeletion and delineate a refined minimal smallest region of overlap (SRO) of approximately 189 kb, representing the narrowest critical interval associated with the 3q27.1 microdeletion phenotype to date. Chromosomal microarray and exome-based CNV analysis confirmed the deletion, which encompasses PSMD2, EIF4G1, and POLR2H but excludes AP2M1 and DVL3. The patient exhibited severe intrauterine growth restriction, microcephaly, global developmental delay, and mild dysmorphism, consistent with the established 3q27.1 phenotype. PSMD2 encodes a non-ATPase regulatory subunit of the 26S proteasome, and its loss may disrupt proteasome-mediated protein turnover and neuronal homeostasis. Comparison with previously published cases and an overlapping ClinVar variant (ID: 60129) with similar features supports the pathogenicity of this minimal deletion. Our findings refine the 3q27.1 critical region, propose PSMD2 haploinsufficiency as a likely molecular mechanism underlying growth and neurodevelopmental defects. Further cases and functional studies are needed to confirm PSMD2 causality and clarify the proteasome-related mechanisms underlying 3q27.1 microdeletion syndrome. - Source: PubMed
Publication date: 2026/03/10
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