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Members of the polo-like kinase (PLK) family are crucial regulators of cell cycle progression, centriole duplication, mitosis, cytokinesis and the DNA damage response. Recent structural and molecular studies have revealed how such processes depend on the tight regulation of PLK abundance, activity, localization and interactions with other proteins, and how dysregulation may be associated with disease.
Large-scale methodologies to facilitate the systematic measurement of protein abundance, translation level, turnover rate, post-translational modification, localization and interaction with other proteins are beginning to enable dynamic assessments of proteomes at the single-cell level.
Nucleotide excision repair (NER) eliminates structurally diverse DNA lesions by repairing helix-distorting damage throughout the genome as well as transcription-blocking lesions. NER defects result in a wide range of disease phenotypes and recent findings have led to a mechanistic model that explains the complex genotype–phenotype correlations of transcription-coupled repair disorders.
Classically associated with ageing and cancer, cellular senescence also seems to function in tissue remodelling during embryonic development and tissue repair, in which senescent cells are cleared before regeneration. Senescence is therapeutically relevant, as it can be either beneficial or detrimental in different diseases.
