ArticleThe Journal of biological chemistry2010
Nucleoredoxin negatively regulates Toll-like receptor 4 signaling via recruitment of flightless-I to myeloid differentiation primary response gene (88).
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Nucleoredoxin Redox Interactions Are Sensitized by Aging and Potentiated by Chronic Alcohol Consumption in the Mouse Liver.Antioxidants (Basel, Switzerland) · 2024Article
- Is Nucleoredoxin a Master Regulator of Cellular Redox Homeostasis? Its Implication in Different Pathologies.Antioxidants (Basel, Switzerland) · 2022Review
- Importance of the renal ion channel TRPM6 in the circadian secretion of renin to raise blood pressure.Nature communications · 2021Article
- Nucleoredoxin Knockdown in SH-SY5Y Cells Promotes Cell Renewal.Antioxidants (Basel, Switzerland) · 2021Article
- Flightless-I is a potential biomarker for the early detection of alcoholic liver disease.Biochemical pharmacology · 2021Article
- Looking Back at the Early Stages of Redox Biology.Antioxidants (Basel, Switzerland) · 2020Review
- Multifunctional Roles of the Actin-Binding Protein Flightless I in Inflammation, Cancer and Wound Healing.Frontiers in cell and developmental biology · 2020Review
- Ethanol targets nucleoredoxin/dishevelled interactions and stimulates phosphatidylinositol 4-phosphate production in vivo and in vitro.Biochemical pharmacology · 2018Article
- Recombinant Leucine-Rich Repeat Flightless-Interacting Protein-1 Improves Healing of Acute Wounds through Its Effects on Proliferation Inflammation and Collagen Deposition.International journal of molecular sciences · 2018Article
- Nucleoredoxin guards against oxidative stress by protecting antioxidant enzymes.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Redox Regulation of Inflammatory Processes Is Enzymatically Controlled.Oxidative medicine and cellular longevity · 2017Review
- Mechanism-based proteomic screening identifies targets of thioredoxin-like proteins.The Journal of biological chemistry · 2015Article
- Nucleoredoxin promotes adipogenic differentiation through regulation of Wnt/β-catenin signaling.Journal of lipid research · 2015Article
- Proteomic analysis of the effect of retinoic acids on the human breast cancer cell line MCF-7.Molecular biology reports · 2014Article
- Attenuation of flightless I improves wound healing and enhances angiogenesis in a murine model of type 1 diabetes.Diabetologia · 2014Article
- Thioredoxins, glutaredoxins, and peroxiredoxins--molecular mechanisms and health significance: from cofactors to antioxidants to redox signaling.Antioxidants & redox signaling · 2013Review
- Glutaredoxin 1 protects dopaminergic cells by increased protein glutathionylation in experimental Parkinson's disease.Antioxidants & redox signaling · 2012Article
- Lysosomal secretion of Flightless I upon injury has the potential to alter inflammation.Communicative & integrative biology · 2012Article
- The Redox System in C. elegans, a Phylogenetic Approach.Journal of toxicology · 2012Article
- Basic principles and emerging concepts in the redox control of transcription factors.Antioxidants & redox signaling · 2011Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously characterized nucleoredoxin (NRX) as a negative regulator of the Wnt signaling pathway through Dishevelled (Dvl). We perform a comprehensive search for other NRX-interacting proteins and identify Flightless-I (Fli-I) as a novel NRX-binding partner. Fli-I binds to NRX and other related proteins, such as Rod-derived cone viability factor (RdCVF), whereas Dvl binds only to NRX. Endogenous NRX and Fli-I in vivo interactions are confirmed. Both NRX and RdCVF link Fli-I with myeloid differentiation primary response gene (88) (MyD88), an important adaptor protein for innate immune response. NRX and RdCVF also potentiate the negative effect of Fli-I upon lipopolysaccharide-induced activation of NF-kappaB through the Toll-like receptor 4/MyD88 pathway. Embryonic fibroblasts derived from NRX gene-targeted mice show aberrant NF-kappaB activation upon lipopolysaccharide stimulation. These results suggest that the NRX subfamily of proteins forms a link between MyD88 and Fli-I to mediate negative regulation of the Toll-like receptor 4/MyD88 pathway.
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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.