ArticleProceedings of the National Academy of Sciences of the United States of America2002
NOSTRIN: a protein modulating nitric oxide release and subcellular distribution of endothelial nitric oxide synthase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed.
- Multiomic single-nucleus profiling reveals cell-type-specific epigenetic and transcriptional dysregulation in major depressive disorder brain.The international journal of neuropsychopharmacology · 2026Article
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- Genetic Basis of Low-Salinity Tolerance in the Pacific Oyster (Crassostrea gigas) as Revealed by Estimation of Genetic Parameters and Genome-Wide Association Study.Marine biotechnology (New York, N.Y.) · 2025Article
- Antagonizing Il10 and Il4 signaling via intracerebral decoy receptor expression attenuates Aβ accumulation.Acta neuropathologica communications · 2025Article
- Recovery of kidney function in acute kidney injury.Journal of nephrology · 2025Review
- Hutchinson-Gilford progeria syndrome alters the endothelial genetic response to laminar shear stress.Frontiers in physiology · 2025Article
- Genomic regions associated with bovine respiratory disease in pacific northwest Holstein cattle.Frontiers in veterinary science · 2025Article
- Promotion of nitric oxide production: mechanisms, strategies, and possibilities.Frontiers in physiology · 2025Review
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- NOSTRIN is involved in benign prostatic hyperplasia via inhibition of proliferation, oxidative stress, and inflammation in prostate epithelial cells.Translational andrology and urology · 2024Article
- Serum Nostrin-A risk factor of death, kidney replacement therapy and acute kidney disease in acute kidney injury.PloS one · 2024Article
- A Scoping Review on Biomarkers of Endothelial Dysfunction in Small Vessel Disease: Molecular Insights from Human Studies.International journal of molecular sciences · 2023Article
- Exome-wide analysis reveals role ofHGG advances · 2023Article
- A "multi-omics" analysis of blood-brain barrier and synaptic dysfunction in APOE4 mice.The Journal of experimental medicine · 2022Article
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- Nitric-Oxide Synthase trafficking inducer (NOSTRIN) is an emerging negative regulator of colon cancer progression.BMC cancer · 2022Article
- Article
- The vital role for nitric oxide in intraocular pressure homeostasis.Progress in retinal and eye research · 2021Review
- Antifungal activity of dendritic cell lysosomal proteins against Cryptococcus neoformans.Scientific reports · 2021Article
- Potential Roles of Endoplasmic Reticulum Stress and Cellular Proteins Implicated in Diabesity.Oxidative medicine and cellular longevity · 2021Review
7 more citing papers are in PubMed but not listed here.
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6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Activity and localization of endothelial nitric oxide synthase (eNOS) is regulated in a remarkably complex fashion, yet the complex molecular machinery mastering stimulus-induced eNOS translocation and trafficking is poorly understood. In a search by the yeast two-hybrid system using the eNOS oxygenase domain as bait, we have identified a previously uncharacterized eNOS-interacting protein, dubbed NOSTRIN (for eNOS traffic inducer). NOSTRIN contains a single polypeptide chain of 506-aa residues of 58 kDa with an N-terminal cdc15 domain and a C-terminal SH3 domain. NOSTRIN mRNA is abundant in highly vascularized tissues such as placenta, kidney, lung, and heart, and NOSTRIN protein is expressed in vascular endothelial cells. Coimmunoprecipitation experiments demonstrated the eNOS-NOSTRIN interaction in vitro and in vivo, and NOSTRIN's SH3 domain was essential and sufficient for eNOS binding. NOSTRIN colocalized extensively with eNOS at the plasma membrane of confluent human umbilical venous endothelial cells and in punctate cytosolic structures of CHO-eNOS cells. NOSTRIN overexpression induced a profound redistribution of eNOS from the plasma membrane to vesicle-like structures matching the NOSTRIN pattern and at the same time led to a significant inhibition of NO release. We conclude that NOSTRIN contributes to the intricate protein network controlling activity, trafficking, and targeting of eNOS.
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