ReviewExperimental dermatology2026
Protein Post-Translational Modifications in UV-Induced Skin Damage.
Review in Experimental dermatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Ultraviolet (UV) irradiation leads to acute photodamage, photoaging and skin cancers. Post-translational modifications (PTMs) represent a key regulatory layer by modulating protein function, localization and interactions under UV stress. This review discusses the mechanistic involvement of PTMs in UV-induced skin damage and summarizes emerging PTM-related photoprotective strategies. Phosphorylation is a central mediator of UV-induced signal transduction, driving activation of the epidermal growth factor receptor (EGFR) and its downstream signalling pathways. Acetylation exerts distinct regulatory effects: histone acetylation primarily regulates transcription of inflammation-related genes and matrix metalloproteinases (MMPs), while non-histone acetylation modulates cellular senescence and mitochondrial antioxidant defence through modification of key proteins. Ubiquitination regulates protein degradation and, through non-degradative modifications, participates in DNA damage recognition and nucleotide excision repair (NER). Furthermore, other PTMs, including methylation, glycosylation, citrullination, SUMOylation and poly(ADP-ribosyl)ation (PARylation), participate in diverse regulatory processes during UV-induced cutaneous alterations. Experimental and emerging interventions associated with PTMs in UV-induced skin damage range from natural extracts to small-molecule agents and mainly include upstream-level modulation of oxidative stress, metabolic status or key effector protein function, as well as enzyme-level modulation of PTM writers and erasers. Different classes of PTMs contribute to UV-induced skin damage through distinct regulatory mechanisms. Further studies should explore the roles of emerging and less-characterized PTMs and evaluate interventions targeting PTM-regulating enzymes in physiologically relevant skin models.
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