Publications by authors named "K G Wiman"
Article Synopsis
- - The study investigates early biochemical events in apoptosis using a novel method called IMPRINTS-CETSA, which focuses on the interaction of proteins during the initial stages of cell death.
- - Researchers analyzed five types of cancer drugs and found that the early stages of apoptosis, particularly concerning caspase targets, primarily occur in the peripheral nuclear region rather than in the cytosol.
- - Despite differing mechanisms among the drugs, the findings suggest that they all lead to similar biochemical changes at the nuclear periphery, indicating its importance as a target for enhancing cancer treatment effectiveness.
Mutations in the tumor suppressor gene occur with high prevalence in a wide range of human tumors. A significant fraction of these mutations (around 10%) are nonsense mutations, creating a premature termination codon (PTC) that leads to the expression of truncated inactive p53 protein. Induction of translational readthrough across a PTC in nonsense mutant allows the production of full-length protein and potentially restoration of normal p53 function.
View Article and Find Full Text PDFp53, which is encoded by the most frequently mutated gene in cancer, TP53, is an attractive target for novel cancer therapies. Despite major challenges associated with this approach, several compounds that either augment the activity of wild-type p53 or restore all, or some, of the wild-type functions to p53 mutants are currently being explored. In wild-type TP53 cancer cells, p53 function is often abrogated by overexpression of the negative regulator MDM2, and agents that disrupt p53-MDM2 binding can trigger a robust p53 response, albeit potentially with induction of p53 activity in non-malignant cells.
View Article and Find Full Text PDFThe retinoblastoma protein (Rb) is encoded by the RB1 tumor suppressor gene. Inactivation of RB1 by inherited or somatic mutation occurs in retinoblastoma and various other types of tumors. A significant fraction (25.
View Article and Find Full Text PDFThe and tumour suppressor genes are inactivated by nonsense mutations in a significant fraction of human tumours. nonsense mutatant tumours account for approximately one million new cancer cases per year worldwide. We have screened chemical libraries with the aim of identifying compounds that induce translational readthrough and expression of full-length p53 protein in cells with nonsense mutation in this gene.
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