ArticleInternational journal of molecular sciences2023
ARL6IP5 Ameliorates α-Synuclein Burden by Inducing Autophagy via Preventing Ubiquitination and Degradation of ATG12.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- ARL6IP5 in cancers: bidirectional function and therapeutic value.Cancer gene therapy · 2025Review
- ADP ribosylation factor-like GTPase 6-interacting protein 5 (Arl6IP5) is an ER membrane-shaping protein that modulates ER-phagy.The Journal of biological chemistry · 2025Article
- A novel ER stress regulator ARL6IP5 induces reticulophagy to ameliorate the prion burden.Autophagy · 2025Article
- Deciphering the role of sphingolipid metabolism in the immune microenvironment and prognosis of esophageal cancer via single-cell sequencing and bulk data analysis.Discover oncology · 2024Article
- DNA methylation in peripheral blood is associated with renal aging and renal function decline: a national community study.Clinical epigenetics · 2024Article
- Autophagy and UPS pathway contribute to nicotine-induced protection effect in Parkinson's disease.Experimental brain research · 2024Article
- Neurodegenerative Disease: From Molecular Basis to Therapy.International journal of molecular sciences · 2024Article
- Neural Marker Expression in Adipose-Derived Stem Cells Grown in PEG-Based 3D Matrix Is Enhanced in the Presence of B27 and CultureOne Supplements.International journal of molecular sciences · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Recent advanced studies in neurodegenerative diseases have revealed several links connecting autophagy and neurodegeneration. Autophagy is the major cellular degradation process for the removal of toxic protein aggregates responsible for neurodegenerative diseases. More than 30 autophagy-related proteins have been identified as directly participating in the autophagy process. Proteins regulating the process of autophagy are much more numerous and unknown. To address this, in our present study, we identified a novel regulator (ARL6IP5) of neuronal autophagy and showed that the level of ARL6IP5 decreases in the brain with age and in Parkinson's disease in mice and humans. Moreover, a cellular model of PD (Wild type and A53T mutant α-synuclein overexpression) has also shown decreased levels of ARL6IP5. ARL6IP5 overexpression reduces α-synuclein aggregate burden and improves cell survival in an A53T model of Parkinson's disease. Interestingly, detailed mechanistic studies revealed that ARL6IP5 is an autophagy inducer. ARL6IP5 enhances Rab1-dependent autophagosome initiation and elongation by stabilizing free ATG12. We report for the first time that α-synuclein downregulates ARL6IP5 to inhibit autophagy-dependent clearance of toxic aggregates that exacerbate neurodegeneration.
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