Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.scib.2024.06.001 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Nuclear paxillin functions as a molecular switch for alternative splicing in neurons during a critical period of brain development.
EMBO J
September 2025
Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
During a critical period of postnatal brain development, neural circuits undergo significant refinement coincident with widespread alternative splicing of hundreds of genes, which undergo altered splice site selection for the generation of isoforms essential for synaptic plasticity. Here, we reveal that neuronal activity-dependent phosphorylation of paxillin at its serine 119 (p-paxillin) acts as a molecular switch in the nucleus for the control of alternative splicing during this period. We show that following NMDA receptor activation, nuclear p-paxillin is recruited to nuclear speckles, where it interacts with splicing factors, such as U2AFs.
View Article and Find Full Text PDFClusters of deep intronic RbFox motifs embedded in large assembly of splicing regulators sequences regulate alternative splicing.
PLoS Genet
September 2025
Neural Development Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, United States of America.
The RbFox RNA binding proteins regulate alternative splicing of genes governing mammalian development and organ function. They bind to the RNA sequence (U)GCAUG with high affinity but also non-canonical secondary motifs in a concentration dependent manner. However, the hierarchical requirement of RbFox motifs, which are widespread in the genome, is still unclear.
View Article and Find Full Text PDFRBM15 Mediated m6A Modification of SRSF1 Inhibits Cuproptosis in Non-Small Cell Lung Cancer by Mediating ATP7B Alternative Splicing.
Kaohsiung J Med Sci
September 2025
Department of Medical Oncology, Haikou People's Hospital, Haikou, Hainan, People's Republic of China.
Inhibition of cuproptosis contributes to the development of non-small cell lung cancer (NSCLC). The expression of RNA-binding motif protein 15 (RBM15) is upregulated in NSCLC. Nonetheless, its relationship with cuproptosis remains unclear.
View Article and Find Full Text PDFExploring the Functional Role of Programmed Death-Ligand 1 (PD-L1) in the Castration-Resistant Prostate Cancer Using Transcriptomic Sequencing Analysis.
Cancer Med
September 2025
The Key Laboratory of Tumor Stem Cell Research of Liaoning Province, Dalian Medical University, Dalian, China.
Background: Prostate cancer is one of the principal malignancies threatening human health, and the development of castration resistance often constitutes a major cause of treatment failure in its management.
Methods: To elucidate the potential association between programmed death-ligand 1 (PD-L1) and castration resistance in prostate cancer, we analyzed the expression levels of PD-L1 in both primary prostate cancer tissues and castration-resistant prostate cancer (CRPC) specimens as well as in corresponding cell lines by using western blots and immunohistochemistry. Then, we explored the specific mechanisms through transcriptomic sequencing technology.
Early Regulation and Alternative Splicing Dynamics in Glucocorticoid Muscle Atrophy Revealed by Temporal Omics in C2C12 Myotubes.
Am J Physiol Cell Physiol
September 2025
Humboldt-University zu Berlin, Berlin, Germany.
Skeletal muscle atrophy and weakness are major contributors to morbidity, prolonged recovery, and long-term disability across a wide range of diseases. Atrophy is caused by breakdown of sarcomeric proteins resulting in loss of muscle mass and strength. Molecular mechanism underlying the onset of muscle atrophy and its progression have been analysed in patients, mice, and cell culture but the complementarity of these model systems remains to be explored.
View Article and Find Full Text PDF