Ask about this productRelated genes to: PURB antibody
- Gene:
- PURB NIH gene
- Name:
- purine rich element binding protein B
- Previous symbol:
- -
- Synonyms:
- PURBETA
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-19
- Date modifiied:
- 2016-06-06
Related products to: PURB antibody
Related articles to: PURB antibody
- Global warming may drive adaptive evolution by influencing natural selection and utilizing temperature-related phenotypic plasticity. However, predicting the evolutionary patterns of phenotypic plasticity under climate change remains a challenge, underscoring the need to elaborate on the underlying genetic and molecular mechanisms. In this study, we focus on the expression plasticity divergence of heat shock protein 90 (), which is temperature responsive and exhibits a strong selective sweep in the upstream noncoding region of two allopatric congeneric oyster species: cold-adapted and warm-adapted . Functional characterization confirmed expression as an ideal proxy for thermotolerance. The evolutionary divergence in constitutive and plastic expression patterns represents adaptation to the mean and variance in habitat temperature, respectively. By combining forward and reverse genetic approaches, four causative loci with G + G × E effects were identified in the promoter regions of . and . , indicating -variations. Moreover, the g.-2291G allele of the causative locus in is specifically bound to by the positive transcription factor purine-rich element binding protein B (PURB), explaining the constitutive expression of . Meanwhile, the response of to thermal stress determines the magnitude of plastic expression in . . This integrative study revealed that -variations interact with -variations and underlie the G × E effect under environmental changes, thereby mediating the divergence in plastic gene expression. Furthermore, we established a paradigm for studying genetic variants and their G × E impacts at a finer resolution, i.e., single-nucleotide level, in nonmodel organisms. The findings may deepen our understanding of the significant role of phenotypic plasticity in modulating adaptive responses and promote predictions of adaptive potential in marine organisms under climate change. - Source: PubMed
Publication date: 2026/03/31
Jiang ZhuxiangWang ChaogangDu MingyangCong RihaoLi AoWang WeiZhang GuofanLi Li - Central carbon metabolism is thought to link reactive oxygen species (ROS) with antibiotic-mediated bacterial death. During enrichment screening of with the first-generation quinolone oxolinic acid, unstable antibiotic-tolerant mutants containing deficiencies in were obtained. Examination of a stable deletion mutant of , a gene functionally related to , revealed reduced lethality of oxolinic acid and ciprofloxacin. This deletion mutation had little effect on the minimal inhibitory concentration (MIC) of quinolones, thereby demonstrating that the observed protection from killing was attributable to antibiotic tolerance. AMP synthesis was blocked by the Δ mutation, and ciprofloxacin tolerance was reversed by exogenous AMP supplementation. Because AMP is a precursor of ATP, interference with ATP synthesis occurs in the Δ mutant. RNA-Seq analysis showed that, prior to antibiotic stress, transcript levels of NADH:quinone oxidoreductase genes were reduced by the deficiency, thereby predisposing to antibiotic tolerance through reduced respiration. During ciprofloxacin exposure, the deficiency also suppressed the surge in expression of tricarboxylic acid (TCA) cycle and ATP synthesis genes, as well as the accumulation of intracellular ATP and ROS. Thus, wild-type PurA, and by extension the downstream enzyme PurB, directs AMP toward an antibiotic-mediated, ROS-dependent death pathway. Overall, defects in PurA/PurB-mediated adenosine ribonucleotides biosynthesis reveal a novel quinolone tolerance mechanism that is initiated outside central carbon metabolism; tolerance is likely attributable to a limited supply of AMP, resulting in reduced ATP synthesis and suppression of ROS accumulation. - Source: PubMed
Publication date: 2026/04/16
Zhu WeiweiNong YuejuanSu JieYang JingwenMa LinaXue YunxinWang DaiNiu JianjunDrlica KarlZhao Xilin - Rapid urbanization and afforestation have substantially altered land surface characteristics in China, with important implications for heterogeneous atmospheric chemistry. Here, we investigate how land-cover changes between 2001 and 2020 influence heterogeneous nitrous acid (HONO) production and its subsequent impacts on total nitrate (TNO = HNO + NO⁻) formation using the Community Multiscale Air Quality (CMAQ) model. To isolate chemical effects, all simulations employed identical 2020 meteorological fields and emissions, while only land-cover-related parameters, including percentage of urban area (PURB) and leaf area index (LAI), were varied in the heterogeneous reaction parameterization. Results showed that surface heterogeneous reactions dominated HONO production, contributing to more than 50% of total concentrations. Urban expansion markedly enhanced HONO levels, with increases of 50.3%, 48.4%, 45.2%, and 38.1% in the Beijing-Tianjin-Hebei (BTH), Yangtze River Delta (YRD), Pearl River Delta (PRD), and Sichuan Basin (SCB), respectively, whereas the influence of vegetation changes was comparatively minor with contributions generally below 5%. Enhanced HONO formation exerted a dual influence on TNO chemistry. During daytime, increased HONO photolysis elevated OH radical levels, accelerating the conversion of NO to HNO and increasing TNO by 0.8, 0.6, and 0.3 μg/m in BTH, YRD, and SCB, respectively. In contrast, at night, heterogeneous HONO formation competed with the NO-NO pathway for NO, decreasing nocturnal TNO by 0.2 μg/m in YRD and 0.3 μg/m in SCB. Meteorological feedbacks induced by land-cover change exerted a relatively minor influence on HONO but tended to offset TNO accumulation (about 0.12 μg/m). In addition, sensitivity simulations with a radiation-dependent uptake coefficient (γ) revealed a clear diurnal contrast in HONO, with enhanced daytime and reduced nighttime concentrations compared to the fixed-γ scheme. These findings demonstrate that urbanization-driven surface transformations play an important role in enhancing heterogeneous HONO chemistry and reshaping TNO formation pathways, underscoring the necessity of incorporating dynamic land-cover characteristics and improved parameterizations into regional air quality models. - Source: PubMed
Publication date: 2026/04/26
Liu YangCao JingyuanAi SiqiLiu YuxiChen JiaxuanZheng Boyue - Community-associated methicillin-resistant (CA-MRSA) is a leading cause of bacteremia, yet the genetic basis for its success in this hostile environment remains poorly defined. In this study, we employed transposon-directed insertion site sequencing (TraDIS) to map the fitness landscape of CA-MRSA strain USA300 JE2 through a genome-wide screening in fresh, immunocompetent human blood. We identified 76 genes required for fitness, including genes involved in respiratory and central carbon metabolisms, heme detoxification, and purine biosynthesis. As validation of fitness genes, competition assays confirmed that individual disruption of , , , , or significantly reduced bacterial fitness in blood. Conversely, inactivation of specific regulators, such as the two-component system, the alternative sigma factor σ, and adhesins, including and , conferred a competitive advantage. These findings provide a genome-scale map of fitness requirements in a physiologically relevant blood model, offering a platform for further investigation of bacterial adaptation to the intravascular environment.IMPORTANCEUnderstanding how maintains fitness in the human bloodstream is essential for explaining its success as an invasive pathogen. This study provides a comprehensive, genome-wide definition of the genes that enable to remain competitive in blood, revealing the key physiological requirements for adaptation to this challenging environment. By identifying genetic functions whose disruption impairs fitness, our findings highlight the specific pathways that sustain adaptation and competitiveness under host-imposed stress. Extending previous genome-scale investigations conducted in other infection niches, this study emphasizes the importance of physiological context in shaping bacterial fitness and identifies conserved cross-fitness determinants shared among lineages. These insights advance our current understanding of how adapts to the bloodstream and strengthen the foundation for future functional and comparative studies on staphylococcal pathophysiology. - Source: PubMed
Publication date: 2026/04/21
Abdelmalek NaderYousief Sally WBojer Martin SOlsen John ERubino SalvatorePaglietti Bianca - The initial steps of the human immunodeficiency virus type 1 (HIV-1) life cycle are regulated by cellular RNA-binding proteins, but only a few have been identified. Here, we developed in virion RNA interactome capture (ivRIC) to comprehensively profile the direct protein interactors of the HIV-1 genomic (g)RNA inside the viral particles. We identified 104 cellular RNA-binding proteins in virions (ivRBPs), many of which are nuclear. We determined the interactome of the viral RBP Rev and discovered that nuclear ivRBPs may associate gRNA in the nucleus and continue bound after the genesis of the viral particles. We also observed that ivRBPs are not incorporated into viral particles based on their abundance, but likely through selective mechanisms. Moreover, we show that the ivRBPs PURA and its homolog PURB control HIV-1 particle infectivity and engage with several viral proteins and key elements within HIV-1 gRNA, showcasing the importance of ivRBPs for HIV-1 infection. - Source: PubMed
Publication date: 2026/04/07
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