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RecA deletion disrupts protein homeostasis, leading to deamidation, oxidation, and impaired glycolysis in .
Appl Environ Microbiol
December 2024
School of Medicine, Nankai University, Tianjin, Tianjin, China.
is a foodborne pathogen linked to severe infections in infants and often associated with contaminated powdered infant formula. The RecA protein, a key player in DNA repair and recombination, also influences bacterial resilience and virulence. This study investigated the impact of deletion on the pathogenicity and environmental stress tolerance of BAA-894.
View Article and Find Full Text PDFInteractions between epithelial mesenchymal plasticity, barrier dysfunction and innate immune pathways shape the genesis of allergic airway disease.
Expert Rev Respir Med
January 2025
School of Medicine and Public Health, University of Wisconsin Madison, Madison, WI, USA.
Introduction: In genetically predisposed individuals, exposure to aeroallergens and infections from RNA viruses shape epithelial barrier function, leading to Allergic Asthma (AA). Here, activated pattern recognition receptors (PRRs) in lower airway sentinel cells signal epithelial injury-repair pathways leading to cell-state changes [epithelial mesenchymal plasticity (EMP)], barrier disruption and sensitization.
Areas Covered: 1.
Post-translational modifications on protein VII are important during the early stages of adenovirus infection.
J Virol
December 2024
Department of Microbiology, University of Washington School of Medicine, Seattle, Washington, USA.
Unlabelled: Due to the importance of post-translational modification (PTM) in cellular function, viruses have evolved to both take advantage of and be susceptible to such modification. Adenovirus encodes a multifunctional protein called protein VII, which is packaged with the viral genome in the core of virions and disrupts host chromatin during infection. Protein VII has several PTMs whose addition contributes to the subnuclear localization of protein VII.
View Article and Find Full Text PDFProgressive lung fibrosis: reprogramming a genetically vulnerable bronchoalveolar epithelium.
J Clin Invest
January 2025
Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Idiopathic pulmonary fibrosis (IPF) is etiologically complex, with well-documented genetic and nongenetic origins. In this Review, we speculate that the development of IPF requires two hits: the first establishes a vulnerable bronchoalveolar epithelium, and the second triggers mechanisms that reprogram distal epithelia to initiate and perpetuate a profibrotic phenotype. While vulnerability of the bronchoalveolar epithelia is most often driven by common or rare genetic variants, subsequent injury of the bronchoalveolar epithelia results in persistent changes in cell biology that disrupt tissue homeostasis and activate fibroblasts.
View Article and Find Full Text PDFTransitioning From Nusinersen to Risdiplam for Spinal Muscular Atrophy in Clinical Practice: A Single-Center Experience.
Muscle Nerve
January 2025
Center for Gene Therapy, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, Ohio, USA.
Background: Nusinersen and risdiplam are U.S. Food and Drug Administration (FDA)-approved treatments for spinal muscular atrophy (SMA).
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