Is Nucleoredoxin a Master Regulator of Cellular Redox Homeostasis? Its Implication in Different Pathologies

Nucleoredoxin (NXN), an oxidoreductase enzyme, contributes to cellular redox homeostasis by regulating different signaling pathways in a redox-dependent manner. By interacting with seven proteins so far, namely disheveled (DVL), protein phosphatase 2A (PP2A), phosphofructokinase-1 (PFK1), translocat...

Full description

Saved in:
Bibliographic Details
Published in:Antioxidants 2022-03, Vol.11 (4), p.670
Main Authors: Idelfonso-García, Osiris Germán, Alarcón-Sánchez, Brisa Rodope, Vásquez-Garzón, Verónica Rocío, Baltiérrez-Hoyos, Rafael, Villa-Treviño, Saúl, Muriel, Pablo, Serrano, Héctor, Pérez-Carreón, Julio Isael, Arellanes-Robledo, Jaime
Format: Article
Language:English
Subjects:
Alzheimer's disease
Ca2+/calmodulin-dependent protein kinase II
Calcium-binding protein
Calmodulin
Cell cycle
Chemical bonds
Diabetes mellitus
Endoplasmic reticulum
Enzymes
Glycolysis
Homeostasis
Innate immunity
Kinases
Liver cancer
Liver diseases
MyD88 protein
Neurodegenerative diseases
Neuroplasticity
Organogenesis
Oxidation
Oxidative stress
Oxidoreductase
Phosphofructokinase
Phosphoprotein phosphatase
Phosphorylation
Protein phosphatase
Protein transport
Proteins
redox regulation
Retinitis
Retinitis pigmentosa
Review
Signal transduction
thioredoxin
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Nucleoredoxin (NXN), an oxidoreductase enzyme, contributes to cellular redox homeostasis by regulating different signaling pathways in a redox-dependent manner. By interacting with seven proteins so far, namely disheveled (DVL), protein phosphatase 2A (PP2A), phosphofructokinase-1 (PFK1), translocation protein SEC63 homolog (SEC63), myeloid differentiation primary response gene-88 (MYD88), flightless-I (FLII), and calcium/calmodulin-dependent protein kinase II type alpha (CAMK2A), NXN is involved in the regulation of several key cellular processes, including proliferation, organogenesis, cell cycle progression, glycolysis, innate immunity and inflammation, motility, contraction, protein transport into the endoplasmic reticulum, neuronal plasticity, among others; as a result, NXN has been implicated in different pathologies, such as cancer, alcoholic and polycystic liver disease, liver fibrogenesis, obesity, Robinow syndrome, diabetes mellitus, Alzheimer's disease, and retinitis pigmentosa. Together, this evidence places NXN as a strong candidate to be a master redox regulator of cell physiology and as the hub of different redox-sensitive signaling pathways and associated pathologies. This review summarizes and discusses the current insights on NXN-dependent redox regulation and its implication in different pathologies.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox11040670