ArticleMolecular and cellular biology2013
Nucleophosmin, a critical Bax cofactor in ischemia-induced cell death.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Nucleophosmin 1 proteins as potential therapeutic targets in non-communicable chronic inflammatory diseases: a review of pathophysiological mechanisms.Frontiers in cell and developmental biology · 2026Review
- Nucleolus as a cornerstone linking proliferation and metabolism to cellular responses to stress: involvement of transcription factors MYC and p53.Frontiers in molecular biosciences · 2026Review
- A Phase I Clinical Study and In Vivo Findings with PT-112, a Novel Immunogenic Cell Death-Inducing Small Molecule, in Relapsed or Refractory Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Cancer cell-selective induction of mitochondrial stress and immunogenic cell death by PT-112 in human prostate cell lines.Journal of translational medicine · 2024Article
- The Potential Biotherapeutic Targets of Contrast-Induced Acute Kidney Injury.International journal of molecular sciences · 2023Review
- Proteomic analysis reveals USP7 as a novel regulator of palmitic acid-induced hepatocellular carcinoma cell death.Cell death & disease · 2022Article
- Mechanisms of nucleophosmin (NPM)-mediated regulated cell death elucidated by Hsp70 during renal ischemia.Apoptosis : an international journal on programmed cell death · 2022Article
- The NF-κB Nucleolar Stress Response Pathway.Biomedicines · 2021Review
- T95 nucleophosmin phosphorylation as a novel mediator and marker of regulated cell death in acute kidney injury.American journal of physiology. Renal physiology · 2020Article
- Cross organelle stress response disruption promotes gentamicin-induced proteotoxicity.Cell death & disease · 2020Article
- The nuclear envelope: target and mediator of the apoptotic process.Cell death discovery · 2020Review
- Nucleophosmin Phosphorylation as a Diagnostic and Therapeutic Target for Ischemic AKI.Journal of the American Society of Nephrology : JASN · 2019Article
- Aspirin Prevention of Colorectal Cancer: Focus on NF-κB Signalling and the Nucleolus.Biomedicines · 2017Review
- Blocking peptides and molecular mimicry as treatment for kidney disease.American journal of physiology. Renal physiology · 2017Review
- Cellular and Molecular Mechanisms of AKI.Journal of the American Society of Nephrology : JASN · 2016Review
- Identification of chaperones in a MPPAmerican journal of translational research · 2016Article
- Regulated cell death in AKI.Journal of the American Society of Nephrology : JASN · 2014Review
- Selective 14-3-3γ induction quenches p-β-catenin Ser37/Bax-enhanced cell death in cerebral cortical neurons during ischemia.Cell death & disease · 2014Article
- The molecular basis of myeloid malignancies.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2014Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
We hypothesized that nucleophosmin (NPM), a nucleolar phosphoprotein, is critical for Bax-mediated cell death. To test this hypothesis, Bax activation was induced by metabolic stress. During stress, nucleolar NPM translocated into the cytosol, NPM-Bax complexes formed, and both NPM and Bax accumulated in mitochondria. Expression of a cytosol-restricted NPM mutant (NPM-ΔNLS), but not a nucleus-restricted NPM mutant, increased NPM-Bax complex formation, mitochondrial NPM and Bax accumulation, mitochondrial membrane injury, caspase 3 activation, and ischemia-induced cell death. Coexpression of NPM-ΔNLS with constitutively active Bax mutants caused nearly universal cell death in the absence of metabolic stress, whereas expression of active Bax or NPM-ΔNLS alone did not. A Bax peptide that disrupts NPM-Bax interaction significantly reduced cell death caused by exposure to metabolic inhibitors in vitro and preserved kidney function after ischemia in vivo. Thus, NPM-Bax interaction enhances mitochondrial Bax accumulation, organelle injury, and cell death. NPM-Bax complex formation is a novel target for preventing ischemic tissue injury.
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What OpenQuestion holds
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.