Age-related thymic involution, leading to reduced T cell production, is one of the major causes of immunosenescence. This results in an increased susceptibility to cancers, infections, and autoimmunity and in reduced vaccine efficacy. Here, we identified that the receptor activator of nuclear factor κB (RANK)-RANK ligand (RANKL) axis in the thymus is altered during aging.
View Article and Find Full Text PDFIntroduction: The application of single-cell RNA sequencing has greatly improved our understanding of various cellular and molecular mechanisms involved in physiological and pathophysiological processes. However, obtaining living cells for this technique can be difficult under certain conditions. To solve this problem, the methanol fixation method appeared as a promising alternative for routine clinical use.
View Article and Find Full Text PDFOngoing progress in mRNA-Sequencing technologies has significantly contributed to the refinement of assisted reproductive technologies. However, the prior investigations have predominantly concentrated on alterations in overall gene expression levels, thereby leaving a considerable gap in our understanding of the influence of transcript isoform expression on fundamental cellular mechanisms of oocytes. Given the efficacy of differential transcript usage (DTU) analysis to address such knowledge, we conducted comprehensive DTU analysis utilizing mRNA-Seq datasets of germinal vesicle (GV) and metaphase II (MII) oocytes across six mammalian species from the SRA database, including cow, donkey, horse, human, mouse, and pig.
View Article and Find Full Text PDFBackground And Aim: Fatty liver disease is a common condition, characterized by excess fat accumulation in the liver. It can contribute to more severe liver-related health issues, making it a critical concern in avian and human medicine. Apart from modifying the gene expression of liver cells, the disease also alters the expression of specific transcript isoforms, which might serve as new biological markers for both species.
View Article and Find Full Text PDFThe synthesis of fatty acids from acetyl-coenzyme A (AcCoA) is deregulated in diverse pathologies, including cancer. Here, we report that fatty acid accumulation is negatively regulated by nucleoside diphosphate kinases 1 and 2 (NME1/2), housekeeping enzymes involved in nucleotide homeostasis that were recently found to bind CoA. We show that NME1 additionally binds AcCoA and that ligand recognition involves a unique binding mode dependent on the CoA/AcCoA 3' phosphate.
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