Ask about this productRelated genes to: ABCE1 Blocking Peptide
- Gene:
- ABCE1 NIH gene
- Name:
- ATP binding cassette subfamily E member 1
- Previous symbol:
- RNASEL1, RNASELI, RNS4I
- Synonyms:
- RLI, OABP, RLI1
- Chromosome:
- 4q31.21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-01
- Date modifiied:
- 2016-10-05
Related products to: ABCE1 Blocking Peptide
Related articles to: ABCE1 Blocking Peptide
- Iron is required to support essential cellular processes. Due to diverse and dynamic host environments, the obligate intracellular parasite must adapt to iron-limited conditions. To investigate the adaptations critical to parasite survival under these conditions, we conducted proteomic and metabolomic profiling of cultured in iron-depleted conditions. We find that iron depletion results in remodeling of the parasite proteome and triggers swift translational repression, prior to decreases in the key translational factor ABCE1. In the context of repressed translation, we also observe a significant rewiring of energy metabolism. Iron-depleted have altered mitochondrial morphology and a profound reduction in mitochondrial respiration. Untargeted metabolomics revealed changes in central carbon metabolism, with the accumulation of intermediates of glycolysis and the tricarboxylic acid (TCA) cycle. Stable isotope labeling revealed that iron deprivation leads to a fundamental disconnect between these pathways, with reduced incorporation of glucose-derived carbon into cellular macromolecules and disruption of the TCA cycle. Instead, iron-deprived parasites continued to take up glucose and maintain glycolysis for energy generation. Limiting glucose availability, either in culture media or by genetic ablation of glucose uptake, caused a significant increase in sensitivity to iron restriction. Conversely, the limitation of mitochondrially metabolized glutamine improved parasite fitness in iron-depleted conditions. Together, our results establish iron as a key regulator of parasite translation and metabolic flexibility and demonstrate an increased reliance on glycolysis for energy generation and survival under acute iron deprivation.IMPORTANCEThis study determines the effects of iron deprivation on the parasite . Using proteomics and metabolomics, we reveal iron as a novel regulator of both protein translation and energy metabolism in underpinning the importance of this nutrient for essential cellular processes. We find that iron depletion introduces a metabolic bottleneck, whereby parasites become dependent on glucose as their major carbon source. By modulating the parasite's metabolism by altering carbon source availability, we identify nutrient conditions that improve parasite survival under iron restriction. These data reveal a key role for adaptive plasticity of central carbon metabolism to drive survival under iron-limited conditions. Understanding the interactions between parasite nutrient availability and metabolism allows us both to map the metabolic flexibility of these parasites and identify potential vulnerabilities. - Source: PubMed
Publication date: 2026/04/02
Hanna Jack CShikha ShikhaSloan Megan AHarding Clare R - encodes adenosylmethionine decarboxylase 1 (AMD1), a key enzyme in polyamine biosynthesis. A subset of ribosomes translating the coding sequence read through the stop codon and pause at a second in-frame stop 384 nucleotides downstream, producing a conserved C-terminal extension (C-tail). Despite growing evidence that such cis-acting elements regulate translation of their genes, the molecular mechanism by which the C-tail mediates ribosome stalling remains unclear. Here, we determined the structure of the ribosome nascent chain complex paused by the AMD1 C-tail which traps eukaryotic release factor 1 (eRF1) with the ATP-binding cassette subfamily E member 1 (ABCE1). The nascent chain forms a molecular clamp that positions an arginine hook in the peptidyl-transferase center, occluding the accommodation of the eRF1 GGQ motif thereby hampering translation termination. Analysis of aggregated ribosome profiling data revealed several genes with a pattern of stop codon readthrough followed by ribosome stalling at a specific location, suggesting that regulatory readthrough-stall mechanisms may not be limited to . - Source: PubMed
Publication date: 2026/03/27
Maldosevic EmirBoiocchi Fabio SSwirski Michal IMeiklejohn Kyle AYordanova Martina MBaranov Pavel VJomaa Ahmad - The Baicheng-You chicken is a precious local chicken breed unique to Xinjiang, renowned for its strong stress resistance and excellent meat quality. However, its reproductive performance, particularly low hatching efficiency, severely restricts the industrial development of this breed. This study aims to systematically elucidate the genetic basis of the hatching performance of Baicheng-You chickens to provide a theoretical foundation for molecular breeding. A total of 844 44-week-old Baicheng-You chickens were studied, and key hatching traits such as the viable egg rate (VER), fertilization rate (FR), hatchability of eggs set (HES), hatchability of fertilized eggs (HFE), and chick hatching weight (CHW) were measured. High-density variation maps were constructed using whole-genome resequencing technology, genetic parameters were estimated using a mixed linear model, and genome-wide association studies (GWAS) were conducted to screen for significantly associated SNPs and candidate genes. Genetic parameter estimates revealed that the viable egg rate (VER, = 0.27) and chick hatching weight (CHW, = 0.40) exhibited moderate to high heritability, while the fertilization rate (FR, = 0.07) and hatchability (HES, = 0.02; HFE, = 0.01) showed low heritability. GWAS identified 44 genome-wide significant SNPs ( < 4.36 × 10) and 130 suggestive significant SNPs ( < 8.71 × 10). Gene annotation identified 1,146 candidate genes significantly associated with the traits, including the family genes, , , , and . Functional enrichment analysis indicated that these genes were significantly enriched in pathways closely related to embryonic immunity and developmental regulation, such as "defense response to bacterium," "positive chemotaxis," "cell cycle," "ubiquitin-mediated proteolysis," and the "apelin signaling pathway." This study is the first to systematically reveal the genetic architecture of hatching performance in Baicheng-You chickens at the whole-genome level. The identified key genes and signaling pathways provide new insights into the molecular regulatory mechanisms of embryonic development and hatching efficiency. The findings not only offer important candidate targets for molecular marker-assisted selection in Baicheng-You chickens but also provide valuable genetic information and scientific support for the conservation and sustainable utilization of this unique local genetic resource. - Source: PubMed
Publication date: 2026/03/06
You GaoyunLi HaiyingJiang TinghaoZhao Xiaoyu - Acute myeloid leukemia (AML) is a highly heterogeneous hematologic malignancy, with its pathogenesis closely associated with cellular states at various stages of differentiation. Existing clinical prognostic models often fail to account for this heterogeneity and lack integration of key molecular pathways. This study aimed to characterize AML differentiation-associated heterogeneity at the single-cell level, investigate the role of UNC13D in immune and dedifferentiation states, and develop a prognostic model integrating these features. - Source: PubMed
Publication date: 2026/02/25
Wang ZiqianZhou Daobin - Current pulmonary arterial hypertension (PAH) diagnostic approaches rely on right heart catheterization to measure the mean pulmonary artery pressure (≥ 20 mmHg), but limit early screening. Imaging techniques lack sensitivity for detecting early pulmonary pressure changes and are subject to variability, often resulting in diagnosis at an irreversible stage. The PAH pathogenesis remains incompletely understood, and improved diagnosis and treatment are urgently needed. In the present study, the Gene Expression Omnibus GSE113439 dataset underwent differential expression analysis of mRNA and Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Hub genes were identified using weighted gene co-expression network and protein-protein interaction network analyses. Immune infiltration and correlation analyses were subsequently performed. We established a PAH rat model, validated the expression of hub genes in human pulmonary arterial smooth muscle cells (hPASMCs) and lung tissues of PAH rats using qRT-PCR, and conducted sequencing on the lung tissues of PAH rat models. PAH involved 547 differentially expressed genes. GO and KEGG enrichment analyses revealed that the focal adhesion, vascular smooth muscle contraction, RNA degradation, ferroptosis, and 2-oxocarboxylic acid metabolism pathways were closely associated with PAH development (P < 0.05). PAH patients had significantly upregulated NOP58, DDX21, ABCE1, CDC5L, and HSP90AA1 expression. Memory B cells, CD8 T cells, follicular helper T cells, activated natural killer cells, monocytes, activated mast cells, and neutrophils were significantly different between PAH patients and controls. Neutrophils, macrophages, and NOP58 expression were closely associated. NOP58, DDX21, ABCE1, CDC5L, and HSP90AA1 may be novel PAH diagnostic biomarkers and therapeutic targets. Their clinical applicability should be validated in larger-sample studies to explore gene-guided personalized therapies. - Source: PubMed
Publication date: 2026/02/21
Jia RuohanWang KeLiu YizeMa YuanyingLi YueFan MingweiLi PengfeiWang YuJiang TianciDai LinglingCheng Zhe