ArticleNature communications2020
A kinome-wide screen identifies a CDKL5-SOX9 regulatory axis in epithelial cell death and kidney injury.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- Implant Renal Injury-Responsive Cells to Supplement Erythropoietin and Protect Kidney Injury.MedComm · 2025Article
- Metabolic Stress-Induced Choline Kinase α (CHKA) Activation in Endothelial Subpopulation Contributes to Diabetes-Associated Microvascular Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CDKL5 Deficiency Disorder: Revealing the Molecular Mechanism of Pathogenic Variants.International journal of molecular sciences · 2025Article
- Inhibition of HIF-prolyl hydroxylase promotes renal tubule regeneration via the reprogramming of renal proximal tubular cells.Acta pharmacologica Sinica · 2025Article
- Resazurin dye is an in vivo sensor of kidney tubular function.Kidney international · 2025Article
- A phylogenetic analysis of the CDKL protein family unravels its evolutionary history and supports theFrontiers in cell and developmental biology · 2025Article
- 9-Methylfascaplysin Prevents Neuroinflammation and Synaptic Damage via Cell-Specific Inhibition of Kinases in APP/PS1 Transgenic Mice.CNS neuroscience & therapeutics · 2024Article
- Sustained alterations in proximal tubule gene expression in primary culture associate with HNF4A loss.Scientific reports · 2024Article
- Role of the CDKL1-SOX11 signaling axis in acute kidney injury.American journal of physiology. Renal physiology · 2024Article
- Systematic Evaluation of Tyrosine Kinase Inhibitors as OATP1B1 Substrates Using a Competitive Counterflow Screen.Cancer research communications · 2024Article
- Bacterial Production of CDKL5 Catalytic Domain: Insights in Aggregation, Internal Translation and Phosphorylation Patterns.International journal of molecular sciences · 2024Article
- Novel CDKL5 targets identified in human iPSC-derived neurons.Cellular and molecular life sciences : CMLS · 2024Article
- Traditional Chinese Medicine and renal regeneration: experimental evidence and future perspectives.Chinese medicine · 2024Review
- Epilepsy-linked kinase CDKL5 phosphorylates voltage-gated calcium channel Cav2.3, altering inactivation kinetics and neuronal excitability.Nature communications · 2023Article
- SLC12A8 mediates TKI resistance in EGFR-mutant lung cancer via PDK1/AKT axis.Journal of cancer research and clinical oncology · 2023Article
- Inhibition of retinoic acid signaling in proximal tubular epithelial cells protects against acute kidney injury.JCI insight · 2023Article
- Hepatocyte-specific Sox9 knockout ameliorates acute liver injury by suppressing SHP signaling and improving mitochondrial function.Cell & bioscience · 2023Article
- Article
- Zinc finger protein 24-dependent transcription factor SOX9 up-regulation protects tubular epithelial cells during acute kidney injury.Kidney international · 2023Article
- Discovery of a Potent and Selective CDKL5/GSK3 Chemical Probe That Is Neuroprotective.ACS chemical neuroscience · 2023Article
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23 authors at 7 institutions in 2 countries.
Funding
Abstract
Renal tubular epithelial cells (RTECs) perform the essential function of maintaining the constancy of body fluid composition and volume. Toxic, inflammatory, or hypoxic-insults to RTECs can cause systemic fluid imbalance, electrolyte abnormalities and metabolic waste accumulation- manifesting as acute kidney injury (AKI), a common disorder associated with adverse long-term sequelae and high mortality. Here we report the results of a kinome-wide RNAi screen for cellular pathways involved in AKI-associated RTEC-dysfunction and cell death. Our screen and validation studies reveal an essential role of Cdkl5-kinase in RTEC cell death. In mouse models, genetic or pharmacological Cdkl5 inhibition mitigates nephrotoxic and ischemia-associated AKI. We propose that Cdkl5 is a stress-responsive kinase that promotes renal injury in part through phosphorylation-dependent suppression of pro-survival transcription regulator Sox9. These findings reveal a surprising non-neuronal function of Cdkl5, identify a pathogenic Cdkl5-Sox9 axis in epithelial cell-death, and support CDKL5 antagonism as a therapeutic approach for AKI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.