PURA antibody - N-terminal region (ARP33201_P050)
- Known as:
- PURA (anti-) - N-terminal region (ARP33201_P050)
- Catalog number:
- arp33201_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PURA antibody - N-terminal region (ARP33201_P050)
Related genes to: PURA antibody - N-terminal region (ARP33201_P050)
- Gene:
- PURA NIH gene
- Name:
- purine rich element binding protein A
- Previous symbol:
- -
- Synonyms:
- PURALPHA, PUR1, PUR-ALPHA
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-19
- Date modifiied:
- 2017-09-22
Related products to: PURA antibody - N-terminal region (ARP33201_P050)
Related articles to: PURA antibody - N-terminal region (ARP33201_P050)
- 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 - In this paper, we develop a connectivity-exact bond-resolved framework for quantifying structural accessibility and persistence in drug molecules. Representing a molecule as a heavy-atom graph [Formula: see text] each bond is classified uniquely as either a connectivity-critical Entry-point bond ([Formula: see text]) or a connectivity-preserving Fortress bond ([Formula: see text]) yielding the exact identity [Formula: see text] This exhaustive partition separates fragmentation capacity from invariant scaffold structure without adjustable parameters. To refine the invariance coordinate we introduce Total Structural Entrenchment (TSE) a persistence-weighted functional defined over cycle-supported bonds and modulated by local steric wall contributions [Formula: see text]. The resulting two-parameter embedding [Formula: see text] distinguishes superficial cyclic extent from deeply embedded structural reinforcement and resolves degeneracies inherent in raw bond counts. Metabolic progression is formalized as recursive bridge depletion generating a directed migration across the architectural plane toward a bridge-depleted refractory core. Within this framework scaffold persistence is interpreted as a connectivity-driven contraction governed strictly by graph topology. The resulting invariance-variation embedding establishes a mathematically controlled bond-level representation of structural accessibility and cyclic entrenchment. - Source: PubMed
Devi K NaliniSrinivasa G - Surveillance of severe acute respiratory illness (SARI) in Brazil provides an early warning system for respiratory outbreaks, including COVID-19, and statistical nowcasting methods are vital for correcting long and variable reporting delays that would otherwise hinder timely decision-making. Coherent joint prediction of SARI and COVID-positive SARI in Brazil could improve outbreak response planning and hospital resource management, but most existing nowcasting methods only target one outcome at a time. Furthermore, existing approaches usually focus solely on reconstructing recent incidence rather than forecasting future trends, which could support more proactive risk mitigation. Here, we propose a Bayesian hierarchical framework for joint nowcasting and short-term forecasting of two outcomes, where one is a strict subset of the other. Building on the generalized-Dirichlet-multinomial (GDM) method for correcting delayed reporting, a new beta-binomial component links SARI and COVID-positive counts, while separate conditional GDM components capture their distinct delay patterns. To allow for changes over time in the level of disease and delay distributions, flexible latent effects are included in all model components. Using national surveillance data from 2021 to 2024, we conduct a 20-date rolling prediction experiment across Brazil's 27 federative units. Compared to a well-established Bayesian nowcasting approach, our joint model achieves about one-third lower mean absolute error and continuous ranked probability score for contemporaneous nowcasts, with the largest gains in high-incidence regions. Meanwhile, energy scores indicate improved calibration for joint forecasts of total and COVID-positive SARI relative to comparable independent models. - Source: PubMed
Halliday AlbaStoner OliverEconomou TheoBastos Leonardo Soares - PURA syndrome is a rare genetic disease characterized by significant phenotypic variability. This case report presents a 4-day-old female neonate presenting with hypotonia, feeding difficulties, and other symptoms. Following comprehensive clinical examination, including laboratory tests, imaging studies, and genetic analysis, the patient was diagnosed with PURA syndrome. Whole-exome sequencing was performed on blood samples collected from the patient and her parents, revealing a novel gene mutation [c.463C>G (p.Tyr155Ter), NM_005859.5], which had not been previously recorded in the literature. This case report aims to expand the known genotype of PURA syndrome and support clinicians in early detection and diagnosis. Early diagnosis facilitates immediate initiation of targeted swallowing function assessment and rehabilitation training, prevents aspiration pneumonia, and guides families in genetic counseling to avoid recurrence risk. - Source: PubMed
Publication date: 2026/03/31
Wang Yongxin - PURA-related neurodevelopmental disorder (PURA-NDD) is an ultra-rare genetic condition caused by heterozygous pathogenic variants in the PURA gene, leading to haploinsufficiency of the Pur-α protein, a critical regulator of neuronal development and RNA trafficking. The disorder is characterized by neonatal hypotonia, global developmental delay, intellectual disability, severely impaired speech, epilepsy, feeding difficulties, respiratory dysfunction, and multisystem involvement. Clinical presentation is heterogeneous, with variability in seizure burden, motor milestones, autonomic dysfunction, endocrine abnormalities, and musculoskeletal complications such as scoliosis. Diagnosis relies on molecular confirmation through genome-wide sequencing, with early recognition enabling anticipatory guidance and multidisciplinary management. Current treatment remains supportive and symptom-directed, focusing on seizure control, nutritional support, respiratory care, rehabilitative therapies, and management of associated comorbidities. Evidence for targeted interventions, including ketogenic diet, vagus nerve stimulation, and neuromuscular junction-modulating agents, remains limited to case-based and small-cohort data. Emerging disease-modifying strategies, including adeno-associated virus-mediated gene replacement, antisense oligonucleotide approaches, RNA-targeted therapies, and drug repurposing, are under preclinical investigation. Advances in animal models, epigenetic profiling, and global patient registries are refining genotype-phenotype correlations and informing future clinical trial design. This comprehensive clinical review synthesizes current evidence on the genetics, pathophysiology, clinical spectrum, diagnostic evaluation, management strategies, and evolving therapeutic landscape of PURA-NDD, highlighting practical considerations for clinicians and priorities for translational research. - Source: PubMed
Publication date: 2026/03/13
Afshar SadafAhmed WajihaÇelik Elif ÖzgeYounis Sumayyah SCampbell ColleenPotluri Yamuna Karthika RaoKaur JaskaranMeda Deepak SwaroopManjari Kopparti KKhachikian ArvinLeena JayalekshmiRai Manju