ArticleThe Journal of biological chemistry2011
Nicotinamide mononucleotide adenylyltransferase is a stress response protein regulated by the heat shock factor/hypoxia-inducible factor 1alpha pathway.
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 31 papers.
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Who cites it
31 citing papers in PubMed, 42 citations in OpenAlex.
- Nicotinamide Mononucleotide Adenylyltransferase 1 and NADMetabolites · 2026Review
- Transcriptional regulation of human NMNAT2: insights from 3D genome sequencing and bioinformatics.The FEBS journal · 2026Article
- The Roles of Moonlighting Nicotinamide Mononucleotide Adenylyl Transferases in Cell Physiology.International journal of molecular sciences · 2025Review
- Inhibitors of NADInternational journal of molecular sciences · 2024Review
- Contribution of HIF-1α to Heat Shock Response by Transcriptional Regulation of HSF1/HSP70 Signaling Pathway in Pacific Oyster, Crassostrea gigas.Marine biotechnology (New York, N.Y.) · 2023Article
- Mitochondrial translation deficiency impairs NADThe EMBO journal · 2021Article
- Healthy Lifestyle Recommendations: Do the Beneficial Effects Originate from NADOxidative medicine and cellular longevity · 2020Review
- Loss ofFrontiers in neurology · 2020Article
- MicroRNA miR-1002 Enhances NMNAT-Mediated Stress Response by Modulating Alternative Splicing.iScience · 2019Article
- Review
- Protein-protein interactions of the nicotinamide/nicotinate mononucleotide adenylyltransferase of Leishmania braziliensis.Memorias do Instituto Oswaldo Cruz · 2019Article
- Role of Nicotinamide Adenine Dinucleotide and Related Precursors as Therapeutic Targets for Age-Related Degenerative Diseases: Rationale, Biochemistry, Pharmacokinetics, and Outcomes.Antioxidants & redox signaling · 2019Review
- Enteric Neurodegeneration is Mediated Through Independent Neuritic and Somal Mechanisms in Rotenone and MPP+ Toxicity.Neurochemical research · 2018Article
- NMNAT3 is protective against the effects of neonatal cerebral hypoxia-ischemia.Annals of clinical and translational neurology · 2017Article
- The β-NADOncotarget · 2017Article
- NMNAT: It's an NADCurrent opinion in genetics & development · 2017Review
- Nicotinamide mononucleotide adenylyltransferase promotes hypoxic survival by activating the mitochondrial unfolded protein response.Cell death & disease · 2016Article
- Alternative splicing of Drosophila Nmnat functions as a switch to enhance neuroprotection under stress.Nature communications · 2015Article
- Nicotinamide Mononucleotide Adenylyltransferase 1 Protects Neural Cells Against Ischemic Injury in Primary Cultured Neuronal Cells and Mouse Brain with Ischemic Stroke Through AMP-Activated Protein Kinase Activation.Neurochemical research · 2015Article
- Metabolic Profiles in Ovine Carotid Arteries with Developmental Maturation and Long-Term Hypoxia.PloS one · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Stress responses are cellular processes essential for maintenance of cellular integrity and defense against environmental and intracellular insults. Neurodegenerative conditions are linked with inadequate stress responses. Several stress-responsive genes encoding neuroprotective proteins have been identified, and among them, the heat shock proteins comprise an important group of molecular chaperones that have neuroprotective functions. However, evidence for other critical stress-responsive genes is lacking. Recent studies on the NAD synthesis enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT) have uncovered a novel neuronal maintenance and protective function against activity-, injury-, or misfolded protein-induced degeneration in Drosophila and in mammalian neurons. Here, we show that NMNAT is also a novel stress response protein required for thermotolerance and mitigation of oxidative stress-induced shortened lifespan. NMNAT is transcriptionally regulated during various stress conditions including heat shock and hypoxia through heat shock factor (HSF) and hypoxia-inducible factor 1α in vivo. HSF binds to nmnat promoter and induces NMNAT expression under heat shock. In contrast, under hypoxia, HIF1α up-regulates NMNAT indirectly through the induction of HSF. Our studies provide an in vivo mechanism for transcriptional regulation of NMNAT under stress and establish an essential role for this neuroprotective factor in cellular stress response.
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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.