Andrew S McNeal, Rachel L Belote ... Robert L Judson-Torres
Oncogenic BRAF causes genome duplication and reversible growth arrest in human melanocytes that is conditional on microRNA expression and differentiation state.
Protein kinase A-driven increases in c-MYC protein expression and tumor cell proliferation can be blocked by eIF4A inhibitors, suggesting a potential new treatment option for patients with oncogenic PKA activation.
Roberta Cacioppo, Hesna Begum Akman ... Catherine Lindon
Post-transcriptional regulation of Aurora Kinase A (AURKA) through alternative polyadenylation of its mRNA determines miRNA influence and is a feature of cell cycle-specific AURKA expression whose impairment leads to acquisition of cancer phenotypes.
Extensive periodic regulation of alternative splicing during the cell cycle in genes is linked to cell cycle functions, and involves an auto-inhibitory mechanism that uses the protein kinase CLK1.
Genetic mouse models combined with single-cell RNA sequencing reveal the essential role of SRSF2 in directing MyoD progenitors to distinct skeletal muscle domains and controlling their differentiation through the regulation of targeted genes and alternative splicing during skeletal muscle development.