ArticleCell death and differentiation2021
Aagab acts as a novel regulator of NEDD4-1-mediated Pten nuclear translocation to promote neurological recovery following hypoxic-ischemic brain damage.
Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- E3 Ubiquitin Ligase NEDD4-Mediated CTSB Ubiquitination Prevents Microglial Ferroptosis After Subarachnoid Hemorrhage.Journal of biochemical and molecular toxicology · 2026Article
- ERα Agonist Protects Aged Female Mice From Sevoflurane Neurotoxicity via PTEN Nuclear Translocation.CNS neuroscience & therapeutics · 2026Article
- Inhibition of PTEN nuclear translocation by peptide Tat-K13 attenuates p-JUN-SESN2-AMPK-dependent autophagy and enhances neurological recovery after neonatal hypoxic-ischemic brain damage.Cell & bioscience · 2026Article
- Neuroprotective Effect of Salvianolic Acid C in Neonatal Rats Following Hypoxic-ischemic Brain Damage.Molecular neurobiology · 2025Article
- Occurrence of multiple melanomas in a patient with punctate palmoplantar keratoderma type-1A associated to alpha and gamma adaptin binding protein.JAAD case reports · 2025Article
- Lactate Dehydrogenase A Crotonylation and Mono-Ubiquitination Maintains Vascular Smooth Muscle Cell Growth and Migration and Promotes Neointima Hyperplasia.Journal of the American Heart Association · 2025Article
- VX-765 alleviates motor and cognitive impairments via inhibiting PANoptosis activation in the neonatal rats after hypoxic-ischemic brain damage.Pediatric discovery · 2025Article
- BNIP3-mediated mitophagy attenuates hypoxic-ischemic brain damage in neonatal rats by inhibiting ferroptosis through P62-KEAP1-NRF2 pathway activation to maintain iron and redox homeostasis.Acta pharmacologica Sinica · 2025Article
- WWP1 targeting PTEN for polyubiquitination to promote bone metastasis of luminal breast cancer.Scientific reports · 2024Article
- Known pathogenic gene variants and new candidates detected in sudden unexpected infant death using whole genome sequencing.American journal of medical genetics. Part A · 2024Article
- PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024Review
- DMT1 ubiquitination by Nedd4 protects against ferroptosis after intracerebral hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Bibliometric analysis of PTEN in neurodevelopment and neurodegeneration.Frontiers in aging neuroscience · 2024Article
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- Dihydroartemisinin attenuates hypoxic-ischemic brain damage in neonatal rats by inhibiting oxidative stress.Molecular brain · 2022Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Hypoxic-ischemic encephalopathy (HIE) is a main cause of mortality and severe neurologic impairment in the perinatal and neonatal period. However, few satisfactory therapeutic strategies are available. Here, we reported that a rapid nuclear translocation of phosphatase and tensin homolog deleted on chromosome TEN (PTEN) is an essential step in hypoxic-ischemic brain damage (HIBD)- and oxygen-glucose deprivation (OGD)-induced neuronal injures both in vivo and in vitro. In addition, we found that OGD-induced nuclear translocation of PTEN is dependent on PTEN mono-ubiquitination at the lysine 13 residue (K13) that is mediated by neural precursor cell expressed developmentally downregulated protein 4-1 (NEDD4-1). Importantly, we for the first time identified α- and γ-adaptin binding protein (Aagab) as a novel NEDD4-1 regulator to regulate the level of NEDD4-1, subsequently mediating Pten nuclear translocation. Finally, we demonstrated that genetic upregulation of Aagab or application of Tat-K13 peptide (a short interference peptide that flanks K13 residue of PTEN) not only reduced Pten nuclear translocation, but also significantly alleviated the deficits of myodynamia, motor and spatial learning and memory in HIBD model rats. These results suggest that Aagab may serve as a regulator of NEDD4-1-mediated Pten nuclear translocation to promote functional recovery following HIBD in neonatal rats, and provide a new potential therapeutic target to guide the clinical treatment for HIE.
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