Nek10-flox Mouse

NEK10, a serine/threonine/tyrosine kinase belonging to the NEK (NIMA-related kinases) family, is involved in multiple crucial cellular processes. It has been linked to pathways such as the DNA damage response (DDR), cell cycle regulation, mitochondrial homeostasis, and β -catenin turnover, and is important for maintaining normal cellular functions and organismal homeostasis [1,2,3,4]. Genetic models, especially gene knockout models, are valuable for studying its functions.

In loss-of-function studies, NEK10-deficient cells show increased cellular proliferation by modulating p53-dependent transcriptional output, as NEK10 directly phosphorylates p53 on Y327 [1]. In mitochondrial-related research, NEK10-depleted cells display fragmented mitochondria, changes in mitochondrial reactive oxygen species (ROS) levels, decreased citrate synthase activity, inhibited mitochondrial respiration, and altered mtDNA amplification and content, indicating its role in mitochondrial homeostasis [2,3]. In A549 lung adenocarcinoma cells, deletion of Nek10 leads to β-catenin stabilization, impairing the cells' ability to form tumorspheres, grow in soft agar, and colonize mouse lung tissue [4]. In human airway cultures, inactivation of NEK10 affects motile ciliary proteome, ciliary length, and mucociliary transport, suggesting its role in airway mucociliary clearance [5].

In conclusion, NEK10 plays essential roles in DNA damage response, cell cycle regulation, mitochondrial function, β-catenin turnover, and airway mucociliary clearance. Studies using NEK10 knockout models have provided insights into its functions in these processes, which may have implications for understanding diseases related to these pathways, such as cancer, ciliopathies, and respiratory disorders [1,2,3,4,5].