ArticleMolecular biology of the cell2013
Adenovirus RIDα uncovers a novel pathway requiring ORP1L for lipid droplet formation independent of NPC1.
Article in Molecular biology of the cell, 2013. 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, 40 citations in OpenAlex.
- Loss of HD-PTP function results in lipodystrophy, defective cellular signaling and altered lipid homeostasis.Journal of cell science · 2024Article
- Linking Late Endosomal Cholesterol with Cancer Progression and Anticancer Drug Resistance.International journal of molecular sciences · 2022Review
- Endosomal Cholesterol in Viral Infections - A Common Denominator?Frontiers in physiology · 2021Review
- Role of Lipid Transfer Proteins (LTPs) in the Viral Life Cycle.Frontiers in microbiology · 2021Review
- Adenovirus Reveals New Pathway for Cholesterol Egress from the Endolysosomal System.International journal of molecular sciences · 2020Review
- Targeting defective sphingosine kinase 1 in Niemann-Pick type C disease with an activator mitigates cholesterol accumulation.The Journal of biological chemistry · 2020Article
- Annexin A6 modulates TBC1D15/Rab7/StARD3 axis to control endosomal cholesterol export in NPC1 cells.Cellular and molecular life sciences : CMLS · 2020Article
- NPC1 regulates ER contacts with endocytic organelles to mediate cholesterol egress.Nature communications · 2019Article
- Adenovirus early region 3 RIDα protein limits NFκB signaling through stress-activated EGF receptors.PLoS pathogens · 2019Article
- New Insights to Adenovirus-Directed Innate Immunity in Respiratory Epithelial Cells.Microorganisms · 2019Review
- Bridging the molecular and biological functions of the oxysterol-binding protein family.Cellular and molecular life sciences : CMLS · 2018Review
- Human Adenoviruses, Cholesterol Trafficking, and NF-κB Signaling.Journal of immunological sciences · 2018Article
- Adenovirus Modulates Toll-Like Receptor 4 Signaling by Reprogramming ORP1L-VAP Protein Contacts for Cholesterol Transport from Endosomes to the Endoplasmic Reticulum.Journal of virology · 2017Article
- Interactions between the Coxiella burnetii parasitophorous vacuole and the endoplasmic reticulum involve the host protein ORP1L.Cellular microbiology · 2017Article
- Intracellular Cholesterol Trafficking and Impact in Neurodegeneration.Frontiers in molecular neuroscience · 2017Review
- Manipulation of Host Cholesterol by Obligate Intracellular Bacteria.Frontiers in cellular and infection microbiology · 2017Review
- Oncogenic mutations and dysregulated pathways in obesity-associated hepatocellular carcinoma.Oncogene · 2016Article
- Lysosome and endoplasmic reticulum quality control pathways in Niemann-Pick type C disease.Brain research · 2016Review
- The formation and function of ER-endosome membrane contact sites.Biochimica et biophysica acta · 2016Review
- A murine Niemann-Pick C1 I1061T knock-in model recapitulates the pathological features of the most prevalent human disease allele.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Niemann-Pick disease type C (NPC) is caused by mutations in NPC1 or NPC2, which coordinate egress of low-density-lipoprotein (LDL)-cholesterol from late endosomes. We previously reported that the adenovirus-encoded protein RIDα rescues the cholesterol storage phenotype in NPC1-mutant fibroblasts. We show here that RIDα reconstitutes deficient endosome-to-endoplasmic reticulum (ER) transport, allowing excess LDL-cholesterol to be esterified by acyl-CoA:cholesterol acyltransferase and stored in lipid droplets (LDs) in NPC1-deficient cells. Furthermore, the RIDα pathway is regulated by the oxysterol-binding protein ORP1L. Studies have classified ORP1L as a sterol sensor involved in LE positioning downstream of GTP-Rab7. Our data, however, suggest that ORP1L may play a role in transport of LDL-cholesterol to a specific ER pool designated for LD formation. In contrast to NPC1, which is dispensable, the RIDα/ORP1L-dependent route requires functional NPC2. Although NPC1/NPC2 constitutes the major pathway, therapies that amplify minor egress routes for LDL-cholesterol could significantly improve clinical management of patients with loss-of-function NPC1 mutations. The molecular identity of putative alternative pathways, however, is poorly characterized. We propose RIDα as a model system for understanding physiological egress routes that use ORP1L to activate ER feedback responses involved in LD formation.
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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.