ArticleLife science alliance2021
Mitochondrial Aurora kinase A induces mitophagy by interacting with MAP1LC3 and Prohibitin 2.
Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- How mitochondrial heterogeneity fuels a dynamic organelle ecosystem.Communications biology · 2026Review
- Combining Fret and Super-Resolution Microscopy Reveals Kinase Activation and Mitochondrial Activity at the Nanoscale.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- AURKA/PHB2 signaling drives acquired resistance to KRASCell death discovery · 2026Article
- Development of capsaicin-derived prohibitin ligands to modulate the Aurora kinase A/PHB2 interaction and mitophagy in cancer cells.Communications biology · 2026Article
- Aurora-A-mediated cytosolic localization of Maf1 promotes cell proliferation via regulating mitochondrial function in HCC.Cell death discovery · 2025Article
- Important regulatory role of mitophagy in diabetic microvascular complications.Journal of translational medicine · 2025Review
- Prohibitin 2 ameliorates cisplatin-induced acute kidney injury by modulating mitochondrial homeostasis.Frontiers in physiology · 2025Article
- Phosphoglycerate mutase 5 exacerbates alcoholic cardiomyopathy in male mice by inducing prohibitin-2 dephosphorylation and impairing mitochondrial quality control.Clinical and translational medicine · 2024Article
- Involvement of Endolysosomes and Aurora Kinase A in the Regulation of Amyloid β Protein Levels in Neurons.International journal of molecular sciences · 2024Article
- Dual-specificity phosphatase 1 interacts with prohibitin 2 to improve mitochondrial quality control against type-3 cardiorenal syndrome.International journal of medical sciences · 2024Article
- Genetic interaction mapping of Aurora protein kinases in mouse oocytes.Frontiers in cell and developmental biology · 2024Article
- Aurora Kinase A: Integrating Insights into Cancer, Inflammation, and Infectious Diseases.Gut microbes reports · 2024Review
- Metabolic protein kinase signalling in neuroblastoma.Molecular metabolism · 2023Review
- The mitophagy pathway and its implications in human diseases.Signal transduction and targeted therapy · 2023Review
- To eat or not to eat mitochondria? How do host cells cope with mitophagy upon bacterial infection?PLoS pathogens · 2023Review
- Aurora kinase A/AURKA functionally interacts with the mitochondrial ATP synthase to regulate energy metabolism and cell death.Cell death discovery · 2023Article
- Review
- Pgam5-mediated PHB2 dephosphorylation contributes to endotoxemia-induced myocardial dysfunction by inhibiting mitophagy and the mitochondrial unfolded protein response.International journal of biological sciences · 2023Article
- Exploring the Conformational Landscape and Stability of Aurora A Using Ion-Mobility Mass Spectrometry and Molecular Modeling.Journal of the American Society for Mass Spectrometry · 2022Article
- PGAM5-Mediated PHB2 Dephosphorylation Contributes to Diabetic Cardiomyopathy by Disrupting Mitochondrial Quality Surveillance.Research (Washington, D.C.) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial and haematologic tumours often show the overexpression of the serine/threonine kinase AURKA. Recently, AURKA was shown to localise at mitochondria, where it regulates mitochondrial dynamics and ATP production. Here we define the molecular mechanisms of AURKA in regulating mitochondrial turnover by mitophagy. AURKA triggers the degradation of Inner Mitochondrial Membrane/matrix proteins by interacting with core components of the autophagy pathway. On the inner mitochondrial membrane, the kinase forms a tripartite complex with MAP1LC3 and the mitophagy receptor PHB2, which triggers mitophagy in a PARK2/Parkin-independent manner. The formation of the tripartite complex is induced by the phosphorylation of PHB2 on Ser39, which is required for MAP1LC3 to interact with PHB2. Last, treatment with the PHB2 ligand xanthohumol blocks AURKA-induced mitophagy by destabilising the tripartite complex and restores normal ATP production levels. Altogether, these data provide evidence for a role of AURKA in promoting mitophagy through the interaction with PHB2 and MAP1LC3. This work paves the way to the use of function-specific pharmacological inhibitors to counteract the effects of the overexpression of AURKA in cancer.
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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.