ArticleScientific reports2016
NOGO-A/RTN4A and NOGO-B/RTN4B are simultaneously expressed in epithelial, fibroblast and neuronal cells and maintain ER morphology.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- The expanding role of Nogo-B in hypertension: linking kidney physiology, endothelial function and inflammation.Journal of hypertension · 2026Review
- Edge curvature drives endoplasmic reticulum reorganization and dictates epithelial migration mode.Nature cell biology · 2025Article
- A Pyrido-Quinoxaline Derivative That Downregulates Reticulon 3 Protein Exhibits Potent Antiviral Activity Against Zika Virus.Journal of medical virology · 2025Article
- Identification of Nogo-B as a potential therapeutic target of osteosarcoma via stereochemically selective covalent probes.Cell death & disease · 2025Article
- Challenges and opportunities for the diverse substrates of SPOP E3 ubiquitin ligase in cancer.Theranostics · 2025Review
- Review
- An unexpected role of neurite outgrowth inhibitor A as regulator of tooth enamel formation.International journal of oral science · 2024Article
- Exploring Hypertrophic Cardiomyopathy Biomarkers through Integrated Bioinformatics Analysis: Uncovering Novel Diagnostic Candidates.Cardiology research and practice · 2024Article
- EndothelialCells · 2022Article
- IFITM3 restricts virus-induced inflammatory cytokine production by limiting Nogo-B mediated TLR responses.Nature communications · 2022Article
- The endoplasmic reticulum adopts two distinct tubule forms.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Hypoxia and the integrated stress response promote pulmonary hypertension and preeclampsia: Implications in drug development.Drug discovery today · 2021Review
- The Regulatory Role of Reticulons in Neurodegeneration: Insights Underpinning Therapeutic Potential for Neurodegenerative Diseases.Cellular and molecular neurobiology · 2021Review
- RTN4B interacting protein FAM134C promotes ER membrane curvature and has a functional role in autophagy.Molecular biology of the cell · 2021Article
- The Implication of Reticulons (RTNs) in Neurodegenerative Diseases: From Molecular Mechanisms to Potential Diagnostic and Therapeutic Approaches.International journal of molecular sciences · 2021Review
- Review
- Reticulon-3 Promotes Endosome Maturation at ER Membrane Contact Sites.Developmental cell · 2021Article
- Axonal Endoplasmic Reticulum Dynamics and Its Roles in Neurodegeneration.Frontiers in neuroscience · 2020Review
- RNA-seq analysis identifies cytoskeletal structural genes and pathways for meat quality in beef.PloS one · 2020Article
- Anti‑Nogo‑A antibody promotes brain function recovery after cardiopulmonary resuscitation in rats by reducing apoptosis.Molecular medicine reports · 2020Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reticulons (RTNs) are a large family of membrane associated proteins with various functions. NOGO-A/RTN4A has a well-known function in limiting neurite outgrowth and restricting the plasticity of the mammalian central nervous system. On the other hand, Reticulon 4 proteins were shown to be involved in forming and maintaining endoplasmic reticulum (ER) tubules. Using comparative transcriptome analysis and qPCR, we show here that NOGO-B/RTN4B and NOGO-A/RTN4A are simultaneously expressed in cultured epithelial, fibroblast and neuronal cells. Electron tomography combined with immunolabelling reveal that both isoforms localize preferably to curved membranes on ER tubules and sheet edges. Morphological analysis of cells with manipulated levels of NOGO-B/RTN4B revealed that it is required for maintenance of normal ER shape; over-expression changes the sheet/tubule balance strongly towards tubules and causes the deformation of the cell shape while depletion of the protein induces formation of large peripheral ER sheets.
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