Ask about this productRelated genes to: EIF2S1 antibody
- Gene:
- EIF2S1 NIH gene
- Name:
- eukaryotic translation initiation factor 2 subunit alpha
- Previous symbol:
- EIF2
- Synonyms:
- EIF-2alpha, EIF2A
- Chromosome:
- 14q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-03-04
- Date modifiied:
- 2016-10-05
Related products to: EIF2S1 antibody
Related articles to: EIF2S1 antibody
- Clear cell renal cell carcinoma (ccRCC) exhibits a paradoxical fructose metabolism signature characterized by upregulation of the fructose transporter GLUT5 alongside downregulation of the catabolic enzymes (ketohexokinase, aldolase B, and triokinase), a pattern associated with poor prognosis. Functionally, unlike the pro-survival effect of fructose under glucose deprivation, in the presence of glucose, fructose co-treatment suppresses ccRCC cell proliferation, and induces profound mitochondrial dysfunction, including impaired oxidative phosphorylation, loss of membrane potential, excessive mitochondrial superoxide production, reduced mtDNA copy number, and downregulation of mitochondria-encoded electron transport chain subunits (notably ND2 and ND4 of complex I). Mechanistically, co-treatment with glucose and fructose creates a metabolic trap resulting in fructose-1-phosphate accumulation and ATP depletion. This energy crisis drives profound depletion of purine and pyrimidine nucleotide pools, which selectively triggers the PERK-eIF2S1-ATF4-CHOP axis of the integrated stress response, thereby mediating mitochondrial impairment and ultimately sensitizing ccRCC cells to intrinsic apoptosis via BID cleavage and caspase-3 activation under nutrient stress. Pharmacological treatment with the chemical chaperone 4-phenylbutyric acid (4-PBA) or nucleoside supplementation reverses mitochondrial dysfunction and fructose-induced cytotoxicity. The tumor-suppressive effect of fructose is validated in patient-derived organoids and xenograft mouse models, where fructose administration significantly attenuates tumor growth via ER stress. These findings reveal fructose-driven nucleotide depletion and PERK-dependent ER stress leading to mitochondrial dysfunction, which underlies the tumor-suppressive toxicity of fructose and exposes a targetable metabolic vulnerability in ccRCC. - Source: PubMed
Publication date: 2026/08/07
Li NaDing YanhongYu BowenWang YongqiangGao TongbinYin HuiyongLi ZhenhuaLiu ShuzhenYu GuohuaWang Ningning - EIF2S1 (eIF2α, translation initiation surveillance) and PELO (Pelota, ribosome rescue) operate within established ribosome-associated quality control and translation-initiation surveillance pathways. Direct cross-talk between these systems is mediated through ZAK/GCN-mediated eIF2α phosphorylation under ribosome-stall stress. At the transcriptional layer, however, EIF2S1-PELO co-regulation has not been quantitatively characterized. Using pairing-family architectural decomposition on multi-region GTEx co-expression and BA9 prefrontal cortex RNA-seq from Parkinson's disease and control donors (GSE68719, = 44 controls, = 29 PD), we find: (1) EIF2S1 and PELO share near-identical genome-wide co-expression architecture (continuous Weighted Jaccard = 0.914) with substantial top-partner overlap (binary Jaccard at top 5% = 0.490), producing a Type 1 dissociation gap of 0.424, significantly smaller than 200 random gene-pair gaps (mean 0.644, = -2.57, permutation = 0.015), and the lowest gap in a 21-pair quality-control gene panel; (2) the relationship is approximately linear-monotonic (Type 6 Pearson-Spearman gap ≈ 0.004); (3) cellular functional co-dependency in DepMap CRISPR screens is essentially zero (Jaccard = 0.006, gene-effect Pearson = -0.07), consistent with layer separation between regulatory architecture and cellular phenotype; (4) in an exploratory single-cohort comparison of PD versus control prefrontal cortex, the dissociation gap was larger in PD (0.536 versus 0.424 in control), but this between-group difference did not reach statistical significance under a group-label permutation test ( = 0.40; bootstrap 95% CI on the difference [-0.14, 0.29]), so we present it as a hypothesis for replication rather than an established effect. These findings characterize EIF2S1-PELO transcriptional co-regulation as a constitutive architectural feature distinct from the ZAK/GCN-mediated direct mechanism. The constitutive coupling replicated in independent Alzheimer's disease and ALS frontal-cortex cohorts and across microarray and RNA-seq platforms; a disease-associated weakening of the coupling was directionally consistent across all three diseases but did not reach statistical significance. We note that co-expression patterns are consistent with shared upstream regulatory programs but do not by themselves establish direct co-regulation; the architectural findings reported here are correlational at the transcriptional layer. - Source: PubMed
Publication date: 2026/08/10
Harbert Drake H - Most transcriptomic studies in acute myeloid leukemia (AML) have focused on transcriptional regulation, whereas the clinical and biological relevance of translation initiation factors remains insufficiently defined. Eukaryotic translation initiation factor 2 subunit alpha () is a key regulator of translation initiation, but its prognostic significance and association with AML remain unclear. - Source: PubMed
Publication date: 2026/08/05
Hong XiaoyingHuang YingyingWu WeiJiang XiandongLin YanfengXue YanLin Donghong - Osteoarthritis (OA) is a heterogeneous joint disease characterized by cartilage degeneration. The interplay between extracellular matrix (ECM) remodeling, endoplasmic reticulum (ER) stress, and inflammatory signaling in OA pathogenesis remains incompletely understood. This study aimed to identify robust diagnostic biomarkers and explore the mechanistic convergence of key genes in OA cartilage through an integrated transcriptomic framework. - Source: PubMed
Publication date: 2026/06/15
Lv XueyaYu YangFan JiawenGuo LianjiangZhu XiangLi Xingye - Platelets, a crucial source of liquid biopsy samples, play a significant role in the progression of various malignancies, including non-small cell lung cancer (NSCLC). However, specific biomarkers for early-stage NSCLC have not yet been identified. In this study, we employed bioinformatics approaches to identify differentially expressed genes (DEGs) in tumor-educated platelets (TEPs) from NSCLC. Subsequently, we validated these genes using specimens from patients with early-stage lung cancer, highlighting their potential as biomarkers for NSCLC. - Source: PubMed
Publication date: 2026/06/08
Xu ZhenLi WenxinYu YuenengWu HuifangZhang Lin