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The role of memory T cells in type 1 diabetes: Phenotypes, mechanisms, and therapeutic implications.
Autoimmun Rev
January 2025
Trauma Research Center, Shahid Rajaee (Emtiaz) Trauma Hospital, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address:
Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the loss of insulin-producing cells in the pancreatic islets. Patients with T1D have autoreactive CD4 and CD8 T cells that show specific features, indicating previous exposure to self-antigens. Despite that memory T cells are vital components of the adaptive immune system, providing enduring protection against pathogens; individuals with T1D have a higher proportion of memory T cells compared to healthy individuals with naїve phenotypes.
View Article and Find Full Text PDFRNA Methylation Homeostasis in Ocular Diseases: All Eyes on Me.
Prog Retin Eye Res
January 2025
Department of Ophthalmology, Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, State Key Laboratory of Vision Health, China. Electronic address:
RNA methylation is a pivotal epigenetic modification that adjusts various aspects of RNA biology, including nuclear transport, stability, and the efficiency of translation for specific RNA candidates. The methylation of RNA involves the addition of methyl groups to specific bases and can occur at different sites, resulting in distinct forms, such as N6-methyladenosine (mA), N1-methyladenosine (mA), 5-methylcytosine (mC), and 7-methylguanosine (mG). Maintaining an optimal equilibrium of RNA methylation is crucial for fundamental cellular activities such as cell survival, proliferation, and migration.
View Article and Find Full Text PDFThe C-terminal structure of the N6-methyladenosine deaminase YerA and its role in deamination.
Biochem J
January 2025
The Sun Yat-Sen University, Guangzhou, China.
The N6-methyladenine (6mA) modification is an essential epigenetic marker and plays a crucial role in processes, such as DNA repair, replication, gene expression regulation, etc. YerA from Bacillus subtilis is considered a novel class of enzymes capable of catalyzing the deamination of 6mA to produce hypoxanthine. Despite the significance of this type of enzymes in bacterial self-defense systems and potential applications as a gene-editing tool, the substrate specificity, the catalytic mechanism and the physiological function of YerA are currently unclear due to the lack of structural information.
View Article and Find Full Text PDFCXCR4 promotes tumor stemness maintenance and CDK4/6 inhibitors resistance in ER-positive breast cancer.
Breast Cancer Res
January 2025
Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.
Background: CDK4/6 inhibitors have significantly improved the survival of patients with HR-positive/HER2-negative breast cancer, becoming a first-line treatment option. However, the development of resistance to these inhibitors is inevitable. To address this challenge, novel strategies are required to overcome resistance, necessitating a deeper understanding of its mechanisms.
View Article and Find Full Text PDFGreater residential greenness is associated with reduced epigenetic aging in adults.
Sci Rep
January 2025
Office of Research and Development, United States Environmental Protection Agency, 104 Mason Farm Rd., Chapel Hill, NC, 27514, USA.
Potential pathways linking urban green spaces to improved health include relaxation, stress alleviation, and improved immune system functioning. Epigenetic age acceleration (EAA) is a composite biomarker of biological aging based on DNA methylation measurements; it is predictive of morbidity and mortality. This cross-sectional study of 116 adult residents of a metropolitan area in central North Carolina investigated associations between exposure to residential green spaces and EAA using four previously developed epigenetic age formulas.
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