ArticleJournal of natural products2011
Mitochondrial respiration inhibitors suppress protein translation and hypoxic signaling via the hyperphosphorylation and inactivation of translation initiation factor eIF2α and elongation factor eEF2.
Article in Journal of natural products, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Mechanistic Investigation of Adociaquinone and Xestoquinone Derivatives in Breast Cancer Cells.Marine drugs · 2025Article
- Traditional Chinese medicine in the treatment of breast Cancer.Molecular cancer · 2025Review
- Calcium lignosulfonate modulates physiological and biochemical responses to enhance shoot multiplication inPhysiology and molecular biology of plants : an international journal of functional plant biology · 2023Article
- Marine Compounds, Mitochondria, and Malignancy: A Therapeutic Nexus.Marine drugs · 2022Review
- Repurposing FDA approved drugs inhibiting mitochondrial function for targeting glioma-stem like cells.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Article
- Article
- Atovaquone is active against AML by upregulating the integrated stress pathway and suppressing oxidative phosphorylation.Blood advances · 2019Article
- Down-regulation of the mitochondrial matrix peptidase ClpP in muscle cells causes mitochondrial dysfunction and decreases cell proliferation.Free radical biology & medicine · 2016Article
- Novel Redox-Responsive Amphiphilic Copolymer Micelles for Drug Delivery: Synthesis and Characterization.The AAPS journal · 2015Article
- Kalkitoxin inhibits angiogenesis, disrupts cellular hypoxic signaling, and blocks mitochondrial electron transport in tumor cells.Marine drugs · 2015Article
- Chronic ethanol exposure alters the lung proteome and leads to mitochondrial dysfunction in alveolar type 2 cells.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Toxins in botanical dietary supplements: blue cohosh components disrupt cellular respiration and mitochondrial membrane potential.Journal of natural products · 2014Article
- Semisynthetic studies identify mitochondria poisons from botanical dietary supplements--geranyloxycoumarins from Aegle marmelos.Bioorganic & medicinal chemistry · 2013Article
- Glycolysis inhibitor screening identifies the bis-geranylacylphloroglucinol protonophore moronone from Moronobea coccinea.Journal of natural products · 2012Article
- Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Over 20,000 lipid extracts of plants and marine organisms were evaluated in a human breast tumor T47D cell-based reporter assay for hypoxia-inducible factor-1 (HIF-1) inhibitory activity. Bioassay-guided isolation and dereplication-based structure elucidation of an active extract from the Bael tree (Aegle marmelos) afforded two protolimonoids, skimmiarepin A (1) and skimmiarepin C (2). In T47D cells, 1 and 2 inhibited hypoxia-induced HIF-1 activation with IC50 values of 0.063 and 0.068 μM, respectively. Compounds 1 and 2 also suppressed hypoxic induction of the HIF-1 target genes GLUT-1 and VEGF. Mechanistic studies revealed that 1 and 2 inhibited HIF-1 activation by blocking the hypoxia-induced accumulation of HIF-1α protein. At the range of concentrations that inhibited HIF-1 activation, 1 and 2 suppressed cellular respiration by selectively inhibiting the mitochondrial electron transport chain at complex I (NADH dehydrogenase). Further investigation indicated that mitochondrial respiration inhibitors such as 1 and rotenone induced the rapid hyperphosphorylation and inhibition of translation initiation factor eIF2α and elongation factor eEF2. The inhibition of protein translation may account for the short-term exposure effects exerted by mitochondrial inhibitors on cellular signaling, while the suppression of cellular ATP production may contribute to the inhibitory effects following extended treatment periods.
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