ArticleAmerican journal of physiology. Renal physiology2024
Role of the CDKL1-SOX11 signaling axis in acute kidney injury.
Article in American journal of physiology. Renal physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Phosphofurin Acidic Cluster Sorting Protein 2 Alleviates Kidney Fibrosis by Inhibiting Tubular Epithelial Cell G2/M Arrest through Cyclin-Dependent Kinase-Like 1.Journal of the American Society of Nephrology : JASN · 2026Article
- A New Regulatory Pathway of Cell Cycle Arrest Governs Tubular Cell Fate and Fibrosis Development.Journal of the American Society of Nephrology : JASN · 2026Article
- Pathophysiological role of Na-Cl cotransporter in kidneys, blood pressure, and metabolism.Human cell · 2024Review
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Authors and funding
7 authors.
Funding
Abstract
The biology of the cyclin-dependent kinase-like (CDKL) kinase family remains enigmatic. Contrary to their nomenclature, CDKLs do not rely on cyclins for activation and are not involved in cell cycle regulation. Instead, they share structural similarities with mitogen-activated protein kinases and glycogen synthase kinase-3, although their specific functions and associated signaling pathways are still unknown. Previous studies have shown that the activation of CDKL5 kinase contributes to the development of acute kidney injury (AKI) by suppressing the protective SOX9-dependent transcriptional program in tubular epithelial cells. In the current study, we measured the functional activity of all five CDKL kinases and discovered that, in addition to CDKL5, CDKL1 is also activated in tubular epithelial cells during AKI. To explore the role of CDKL1, we generated a germline knockout mouse that exhibited no abnormalities under normal conditions. Notably, when these mice were challenged with bilateral ischemia-reperfusion and rhabdomyolysis, they were found to be protected from AKI. Further mechanistic investigations revealed that CDKL1 phosphorylates and destabilizes SOX11, contributing to tubular dysfunction. In summary, this study has unveiled a previously unknown CDKL1-SOX11 axis that drives tubular dysfunction during AKI.
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