ArticleThe Journal of biological chemistry2011
Iron regulatory protein 1 outcompetes iron regulatory protein 2 in regulating cellular iron homeostasis in response to nitric oxide.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 64 citations in OpenAlex.
- Rust and redemption: iron-sulfur clusters and oxygen in human disease and health.Metallomics : integrated biometal science · 2025Review
- Ferroptosis as a potential molecular mechanism of bipolar disorder.Translational psychiatry · 2025Review
- Nitric Oxide Signaling and Sensing in Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration.Molecular neurodegeneration · 2024Review
- On the Chemical and Biological Characteristics of Multifunctional Compounds for the Treatment of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Aberrant Transferrin and Ferritin Upregulation Elicits Iron Accumulation and Oxidative Inflammaging Causing Ferroptosis and Undermines Estradiol Biosynthesis in Aging Rat Ovaries by Upregulating NF-Κb-Activated Inducible Nitric Oxide Synthase: First Demonstration of an Intricate Mechanism.International journal of molecular sciences · 2022Article
- ACO1 and IREB2 downregulation confer poor prognosis and correlate with autophagy-related ferroptosis and immune infiltration in KIRC.Frontiers in oncology · 2022Article
- Iron regulatory protein 1 promotes ferroptosis by sustaining cellular iron homeostasis in melanoma.Oncology letters · 2021Article
- SARS-CoV-2 Mediated Hyperferritinemia and Cardiac Arrest: Preliminary Insights.Drug discovery today · 2021Review
- Inflaming the Brain with Iron.Antioxidants (Basel, Switzerland) · 2021Review
- Iron Metabolism Disorders for Cognitive Dysfunction After Mild Traumatic Brain Injury.Frontiers in neuroscience · 2021Review
- Differential translational control of 5' IRE-containing mRNA in response to dietary iron deficiency and acute iron overload.Metallomics : integrated biometal science · 2020Article
- Footprinting SHAPE-eCLIP Reveals Transcriptome-wide Hydrogen Bonds at RNA-Protein Interfaces.Molecular cell · 2020Article
- Molecular Mechanisms of Nitric Oxide in Cancer Progression, Signal Transduction, and Metabolism.Antioxidants & redox signaling · 2019Review
- Structural and functional abnormalities in iron-depleted heart.Heart failure reviews · 2019Review
- Article
- Redox Control of the Human Iron-Sulfur Repair Protein MitoNEET Activity via Its Iron-Sulfur Cluster.The Journal of biological chemistry · 2016Article
- Parkinson's Disease: The Mitochondria-Iron Link.Parkinson's disease · 2016Review
- Recent Advances in Multinuclear Metal Nitrosyl Complexes.Coordination chemistry reviews · 2016Article
- The diabetes drug target MitoNEET governs a novel trafficking pathway to rebuild an Fe-S cluster into cytosolic aconitase/iron regulatory protein 1.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, iron regulatory proteins (IRPs) 1 and 2 posttranscriptionally regulate expression of genes involved in iron metabolism, including transferrin receptor 1, the ferritin (Ft) H and L subunits, and ferroportin by binding mRNA motifs called iron responsive elements (IREs). IRP1 is a bifunctional protein that mostly exists in a non-IRE-binding, [4Fe-4S] cluster aconitase form, whereas IRP2, which does not assemble an Fe-S cluster, spontaneously binds IREs. Although both IRPs fulfill a trans-regulatory function, only mice lacking IRP2 misregulate iron metabolism. NO stimulates the IRE-binding activity of IRP1 by targeting its Fe-S cluster. IRP2 has also been reported to sense NO, but the intrinsic function of IRP1 and IRP2 in NO-mediated regulation of cellular iron metabolism is controversial. In this study, we exposed bone marrow macrophages from Irp1(-/-) and Irp2(-/-) mice to NO and showed that the generated apo-IRP1 was entirely responsible for the posttranscriptional regulation of transferrin receptor 1, H-Ft, L-Ft, and ferroportin. The powerful action of NO on IRP1 also remedies the defects of iron storage found in IRP2-null bone marrow macrophages by efficiently reducing Ft overexpression. We also found that NO-dependent IRP1 activation, resulting in increased iron uptake and reduced iron sequestration and export, maintains enough intracellular iron to fuel the Fe-S cluster biosynthetic pathway for efficient restoration of the citric acid cycle aconitase in mitochondria. Thus, IRP1 is the dominant sensor and transducer of NO for posttranscriptional regulation of iron metabolism and participates in Fe-S cluster repair after exposure to NO.
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Registered trials
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.