ArticleMolecular medicine (Cambridge, Mass.)2023
NNAT is a novel mediator of oxidative stress that suppresses ER + breast cancer.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Neuronatin Influences Endothelial Homeostasis and Atherosclerosis via ER-Mitochondria Interactions.Journal of inflammation research · 2026Article
- Article
- Genome-wide DNA methylation changes after 24 hours at high altitude.Environmental epigenetics · 2026Article
- PAR1-mediated Non-periodical Synchronized Calcium Oscillations in Human Mesangial Cells.Function (Oxford, England) · 2024Article
- Altered methylation of imprinted genes in neuroblastoma: implications for prognostic refinement.Journal of translational medicine · 2024Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNeuronatin (NNAT) was recently identified as a novel mediator of estrogen receptor-positive (ER+) breast cancer cell proliferation and migration, which correlated with decreased tumorigenic potential and prolonged patient survival. However, despite these observations, the molecular and pathophysiological role(s) of NNAT in ER + breast cancer remains unclear. Based on high protein homology with phospholamban, we hypothesized that NNAT mediates the homeostasis of intracellular calcium [Ca
methodsTo evaluate the role of NNAT on [Ca
resultsOur data indicate that NNAT localizes predominantly to EndoR and lysosome, and genetic manipulation of NNAT levels demonstrated that NNAT modulates [Ca
conclusionCollectively, these data suggest that NNAT expression is mediated by oxidative stress and acts as a regulator of Ca
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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.