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mA/YTHDF2-mediated mRNA decay targets TGF-β signaling to suppress the quiescence acquisition of early postnatal mouse hippocampal NSCs.
Cell Stem Cell
January 2025
Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania, Philadelphia, PA, USA; Department of Cell and Developmental Biology, Perelman School for Medicine, University of Pennsylvania, Philadelphia, PA, USA; Institute for Regenerative Medicine, University of Pennsylvania, Philadelphia, PA, USA; The Epigenetics Institute, Perelman School for Medicine, University of Pennsylvania, Philadelphia, PA, USA; Department of Neurosurgery, Perelman School for Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address:
Quiescence acquisition of proliferating neural stem cells (NSCs) is required to establish the adult NSC pool. The underlying molecular mechanisms are not well understood. Here, we showed that conditional deletion of the mA reader Ythdf2, which promotes mRNA decay, in proliferating NSCs in the early postnatal mouse hippocampus elevated quiescence acquisition in a cell-autonomous fashion with decreased neurogenesis.
View Article and Find Full Text PDFEvolutionary divergent clusters of transcribed extinct truncated retroposons drive low mRNA expression and developmental regulation in the protozoan Leishmania.
BMC Biol
October 2024
Research Center in Infectious Diseases and Axis of Infectious and Immune Diseases, Research Center of the Centre Hospitalier Universitaire de Québec-Université Laval, QC, Quebec, Canada.
Background: The Leishmania genome harbors formerly active short interspersed degenerated retroposons (SIDERs) representing the largest family of repetitive elements among trypanosomatids. Their substantial expansion in Leishmania is a strong predictor of important biological functions. In this study, we combined multilevel bioinformatic predictions with high-throughput genomic and transcriptomic analyses to gain novel insights into the diversified roles retroposons of the SIDER2 subfamily play in Leishmania genome evolution and expression.
View Article and Find Full Text PDFCo-regulation and synteny of GFM2 and NSA2 links ribosomal function in mitochondria and the cytosol with chronic kidney disease.
Mol Med
October 2024
Diabetes & Obesity, School of Cardiovascular Medicine and Metabolic Sciences, King's College London, London, SE1 1UL, UK.
Article Synopsis
- - The study investigates the relationship between the ribosomal biogenesis factor NSA2 and mitochondrial dysfunction in chronic kidney disease (CKD), linking cytosolic and mitochondrial processes involved in its pathology.
- - Research methods included culturing human renal tubular cells and measuring mRNA levels, protein content, and cellular respiration while analyzing transcriptomic data from existing CKD datasets.
- - Results indicate that both NSA2 and GFM2 express together in a dose-dependent manner influenced by zinc and hyperglycemia, with increased expression observed in CKD patients, highlighting their potential role in mitochondrial function and kidney disease progression.
Inverse correlation between TP53 gene status and PD-L1 protein levels in a melanoma cell model depends on an IRF1/SOX10 regulatory axis.
Cell Mol Biol Lett
September 2024
RECAMO, Masaryk Memorial Cancer Institute, 602 00, Brno, Czech Republic.
Article Synopsis
- PD-L1 expression is a key factor in how cancer cells escape the immune system, and targeting the PD-L1/PD1 interaction is a common immunotherapy for melanoma patients, although many still do not respond.
- This study focused on different human melanoma cell lines with varying p53 status to examine the relationship between p53, PD-L1, and immune responses, using techniques like immunoblotting and flow cytometry.
- Results indicated that the loss of p53 impacts PD-L1 levels through the regulation of IRF1 and SOX10, and influences the ability of natural killer (NK) cells to kill tumor cells, highlighting the complex interplay of these factors in cancer immune response.
Intermittent and mild cold stimulation enhances immune function of broilers via co-regulation of CIRP and TRPM8 on NF-κB and MAPK signaling pathways.
Poult Sci
September 2024
College of Life Science, Northeast Agricultural University, Harbin, 150030, China; Key Laboratory of Chicken Genetics and Breeding, Ministry of Agriculture and Rural Affairs, Harbin, 150030, China. Electronic address:
Improving immune function is an important indicator for establishing cold adaptation in broilers. In the study, to explore the effects and molecular mechanisms of intermittent and mild cold stimulation (IMCS) on the immune function of broilers, CIRP and TRPM8, induced by cold stimulation, as well as the NF-κB and MAPK pathways which play an important role in immune response, were selected to investigate. A total of 192 one-day-old broilers (Ross 308) were selected and randomly divided into the control group (CC) and the cold stimulation group (CS).
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