Ask about this productRelated genes to: PURB Blocking Peptide
- 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 Blocking Peptide
Related articles to: PURB Blocking Peptide
- 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
Garcia-Moreno ManuelEmbarc-Buh AzmanTruman RobinNoerenberg MarkoIselin LouisaChen HonglinLenz Caroline ELee Jeffrey YDicker KateShetty Snehith DyavariPalmalux NatashaGu QuanSohier Thibault J MJärvelin Aino IKamel WaelRuscica VincenzoRicci Emiliano PDavis IlanMohammed ShabazCastello Alfredo - MYB is a master transcription factor for the hematopoietic system, and its dysregulation drives the development and therapy resistance of leukemia. However, the mechanisms of MYB regulation and MYB-related therapy resistance are still unclear. Here, we identified two bidirectional enhancer RNAs (eRNAs), MY34UE-AS and MY34UE-S, transcribed from the -34 kb enhancer region of MYB. Both eRNAs promote MYB transcription, proliferation, and migration in human leukemia cells, although through different MYB promoters. MY34UE-AS physically interacts with PURB that binds near MYB TSS2, promoting long-range looping between downstream -34 kb enhancer elements and TSS2, ultimately activating TSS2. While MY34UE-S facilitates DNA looping between upstream -34 kb enhancer elements and TSS1, promoting TSS1 transcription. TSS2, but not TSS1, activity increases in drug resistant leukemia cells, resulting increased expression of N-terminally truncated MYB (ΔN MYB) when total MYB remains unaltered. Compared to full-length MYB, ΔN MYB more potently promotes drug resistance through FTH1 and EZH2 pathway, and targeting MY34UE-AS more efficiently alleviates drug resistance than targeting MY34UE-S. The above relationship of MY34UE-AS/MY34UE-S, TSS2/TSS1, and prognosis was also verified in clinical leukemia samples. For the first time we provide the mechanisms underlying promoter usage of MYB and MYB TSS2 mediated drug resistance in human leukemia. - Source: PubMed
Publication date: 2026/01/22
Wang YuchengWang XiangLi MengjiaSong HongkuanLiu ChaoShi MengjieTao XiaoxiaoShen SiyuLi XinyuFang HuiyingZhou ZhenhuaZhang JunfangHan Bingshe