Ask about this productRelated genes to: EIF6 Blocking Peptide
- Gene:
- EIF6 NIH gene
- Name:
- eukaryotic translation initiation factor 6
- Previous symbol:
- EIF3A, ITGB4BP
- Synonyms:
- p27BBP, b(2)gcn
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-24
- Date modifiied:
- 2016-10-05
Related products to: EIF6 Blocking Peptide
Related articles to: EIF6 Blocking Peptide
- Lung adenocarcinoma (LUAD) is a leading cause of cancer-related mortality, with hypoxia contributing to tumor progression and treatment resistance. Identifying hypoxia-related biomarkers could enhance prognosis and therapeutic strategies for LUAD. - Source: PubMed
Publication date: 2026/06/03
Alghamdi BandarRocha Sonia - Evidence for a causal role of DNA methylation sites (CpGs) in type 2 diabetes and glycaemic traits is limited due to the cross-sectional nature of many epigenome-wide association studies (EWAS). In addition, epigenetic studies in West African populations are particularly sparse, despite the high and rising burden of type 2 diabetes in these populations. Hence, we aimed to identify CpGs causally associated with type 2 diabetes among West Africans by leveraging Mendelian randomisation (MR) analysis and longitudinal data. - Source: PubMed
Publication date: 2026/04/24
Meeks Karlijn A Cvan der Linden Eva LBentley Amy RDoumatey Ayo PHenneman PeterFranceschini NoraAssimes Themistocles LChilunga Felix PHayfron-Benjamin Charles FOwusu-Dabo EllisChen GuanjieAgyemang CharlesAdeyemo Adebowale ARotimi Charles N - Eukaryotic initiation factor 6 (eIF6) is an essential regulator of ribosome biogenesis that prevents the premature association of the 60S and 40S ribosomal subunits. eIF6 eviction from nascent 60S particles, mediated by the ribosome biogenesis factors SBDS and EFL1, is required for the formation of translationally competent 80S ribosomes. SBDS and EFL1 deficiencies cause Shwachman-Diamond syndrome (SDS), a ribosomopathy mainly characterized by exocrine pancreatic insufficiency, bone marrow failure and a predisposition to hematological malignancies. Somatic mutations that reduce the amount of eIF6 (e.g., nonsense mutation, deletion) or its ability to bind to the 60S subunit (e.g., N106S missense mutation) are frequently found in hematopoietic cells of SDS individuals. These somatic mutations represent indirect somatic genetic rescue (SGR) in the context of SDS, as they increase cellular fitness to cause clonal expansion and are associated with clinical improvement in some cases. However, the functional consequences of these eIF6 mutations in human SDS cells have never been reported to date. - Source: PubMed
Publication date: 2026/04/06
Bertrand AlexisPage Sarah LePirabakaran VithuraKermasson LaëtitiaBrunet ErikaDonadieu JeanGleizes Pierre-EmmanuelO'Donohue Marie-FrançoiseRevy Patrick - Shwachman-Diamond syndrome (SDS) is a rare genetic disorder characterized by pancreatic insufficiency and neutropenia. While most cases are linked to mutations in the SBDS gene, some involve mutations in the GTPase EFL1. This protein works with SBDS to release the anti-association factor eIF6 from the 60S ribosomal subunit during ribosome biogenesis. The pathogenic EFL1 R1095Q mutant (R1086Q in yeast) exhibits altered guanine nucleotide recognition and impaired eIF6 release, prompting an investigation into its structural consequences. Using the yeast Efl1 orthologue in X-ray hydroxyl radical footprinting experiments, we tracked changes in solvent accessibility caused by the mutation. Although the mutation is situated in domain IV, widespread conformational changes were observed across the protein, particularly in domain I, suggesting a long-range intramolecular communication. Strikingly, the growth defect caused by the pathogenic mutation was rescued by a second mutation located in a allosteric pathway that spans from the nucleotide-binding pocket to domain IV. This compensatory mutation restored proper nuclear localization of eIF6 (Tif6 in yeast). These findings reveal that the R1086Q mutation disrupts a structural communication network within Efl1, impairing the conformational dynamics required for its activity. The loss of this coordination likely underlies the ribosome maturation defects observed in SDS cases linked to EFL1, offering new insights into the molecular basis of the disease. - Source: PubMed
Zúñiga-Domínguez Jonathan AJain RohitGonzález-Andrade MartínFarquhar Erik RChance Mark RGijsbers AbrilSánchez-Puig Nuria - Small cell lung carcinoma (SCLC) is an aggressive neuroendocrine cancer that rapidly develops resistance to platinum-based chemotherapy. A key feature of SCLC is its ability to switch between neuroendocrine (NE) and non-neuroendocrine (non-NE) states, a process linked to therapeutic failure, yet the underlying mechanisms driving this plasticity remain incompletely understood. Here, we show that the translation initiation factor eIF6 is a critical regulator of non-NE transdifferentiation in SCLC. eIF6 expression is consistently upregulated in non-NE states across cell lines, mouse models, and patient samples, accompanied by global remodelling of the translational landscape. Mechanistically, eIF6 dissociates from ribosomes and interacts with the CD104-FAK complex, leading to MAPK pathway activation. Intervening eIF6 suppresses non-NE transdifferentiation and enhances SCLC chemotherapy sensitivity in vitro and in vivo. These findings position the eIF6-CD104-FAK axis as a prognostic marker and therapeutic target, offering a potential strategy to mitigate SCLC resistance. - Source: PubMed
Publication date: 2026/02/24
Peng HaoningWang ZhileWang MengyaoDing ZheyuLi KaixiuWang YuqingYu XuejiaoSong SiyangDeng YulanLiu YiPu QiangLi LuCerezo MichaelWang WeiyaLiu LunxuShen Shensi