ABCE1 antibody
- Known as:
- ABCE1 (anti-)
- Catalog number:
- orb101639
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ABCE1 antibody
Related genes to: ABCE1 antibody
- 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 antibody
Related articles to: ABCE1 antibody
- The ATP-binding cassette E1 (ABCE1) protein is an essential factor for ribosome recycling, splitting post-termination ribosomes into subunits for subsequent rounds of translation. Despite high conservation, human ABCE1 (hABCE1) fails to functionally complement the depletion of its essential yeast homolog, Rli1. In this study, we leveraged this species-specificity to dissect the functional architecture of ABCE1. Through analysis of yeast-human chimeric proteins, we identified the N-terminal nucleotide-binding domain (NBD1) as the primary determinant of this incompatibility. To further investigate, we isolated multiple hABCE1 point mutants (revertants) that successfully restored yeast growth. We then developed a novel dual-luciferase reporter assay to quantify aberrant translation reinitiation in the 3'UTR, an event recognized as a direct consequence of ABCE1 deficiency. Notably, while the revertant mutants rescued yeast viability, they failed to suppress aberrant reinitiation, exhibiting levels equivalent to the nonfunctional hABCE1. This genetic uncoupling of viability from the suppression of reinitiation suggests that the canonical ribosome recycling function required for cell growth and the role in preventing aberrant reinitiation have distinct functional thresholds or are genetically separable aspects of ABCE1 activity. - Source: PubMed
Publication date: 2026/08/31
Nakata ErikoLi YuxinEndo KeiIto Koichi - Extracellular vesicles (EVs) mediate intercellular communication within the tumour microenvironment by carrying cargoes from paracrine parent cells. EVs have attracted great research interest for their ability to carry nucleic acids into recipient cells and modulate cellular functions. However, previous studies have largely focused on RNA sequence information rather than RNA structure features. Here, we observed that EVs derived from colorectal cancer cells are enriched with endogenous double‑stranded RNA (dsRNA), a danger‑associated molecular pattern (DAMP) that leads to the activation of dsRNA‑sensing pathways in recipient cells. Crucially, we investigated the specific crosstalk between tumour-derived EVs and circulating platelets. As anucleate cells, platelets are uniquely suited models for isolating the effects of exogenous nucleic acids. Our analysis reveals that endogenous dsRNA from tumour EVs activates the platelet OAS-RNASEL innate immune ribonuclease cascade and the RNASEL/ABCE1/PELO axis, resulting in the decay of ribosomal protein mRNAs. This study, spanning from clinical observation to mechanistic validation, uncovers a novel pathway of tumour-platelet communication. We identify EV-enriched endogenous dsRNA as a functional mediator that enables tumour cells to directly reprogram platelet transcriptomes, revealing a new dimension of tumour-immune modulation. - Source: PubMed
Sun GaogeTao YuhuanLiu ZihanZhang KaixiangZuo ShuaiChen ShanwenNing ShufangZhang TianyiWang PengyuanZhang YingLu Zhi JohnYin Hang Hubert - Colorectal cancer (CRC) remains a leading cause of cancer-related death, highlighting an unmet need for robust, mechanistically grounded prognostic biomarkers. Through an integrative multi-omics approach, we identified and validated a novel three-gene signature for CRC. Utilizing paired tumor and adjacent tissues from 15 patients, public datasets (TCGA, GSE231559), and machine learning (LASSO, SVM-RFE), we derived a signature comprising ABCE1, ATAD5, and FUT4. These genes were consistently upregulated in tumors, as confirmed by qPCR, and are functionally linked to core oncogenic pathways: ABCE1 (protein synthesis/immune modulation), ATAD5 (DNA replication stress response), and FUT4 (cell adhesion/immune evasion). The signature demonstrated high diagnostic accuracy (AUC 0.85) and significant prognostic value, stratifying patients into distinct risk groups with divergent survival outcomes. Single-cell RNA-seq analysis localized expression to specific cellular compartments, while immune deconvolution revealed a correlated macrophage-dominated microenvironment. A clinically interpretable nomogram was developed with excellent calibration. This study establishes a compact, biologically coherent three-gene signature as a promising tissue-based molecular classifier for CRC, offering novel insights into the intertwined mechanisms of metabolism, genomic instability, and immune suppression, and presenting potential targets for therapeutic development. - Source: PubMed
Publication date: 2026/06/18
Wang YongWang TianbingHe JianZhang TaoJin RongChen DalongHu ZhiqiPang QingLiu Huichun - Ticks are major ectoparasites that significantly impact livestock productivity worldwide. With the growing resistance to synthetic acaricides and increasing concerns about environmental and human safety, identifying effective and ecofriendly alternatives has become a pressing need. This study evaluated the fumigant and contact toxicities of ylang-ylang (Cananga odorata) essential oil (EO) and three plant-derived compounds, lilial, cinene, and α-amylcinnamaldehyde, against Haemaphysalis doenitzi and explored their underlying mechanisms of action. - Source: PubMed
Publication date: 2026/06/08
Zhang SongboGao ZhihuaYang BoyuLiu XintongLu ChenxiaoFeng HaokunZhu PengxuLiang ZihanGhonaim Ahmed HYang Xiaolong - 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