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
- 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 - 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