ArticleAmino acids2016
Co-regulation of mitochondrial respiration by proline dehydrogenase/oxidase and succinate.
Article in Amino acids, 2016. 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 52 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.
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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
52 citing papers in PubMed.
- Metabolomic Classification of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome via Explainable Ensemble Learning and Pareto-Guided Feature Selection.International journal of molecular sciences · 2026Article
- CoQExperimental & molecular medicine · 2026Review
- Consumption of L-Proline as Energy Substrate by Cultured Primary Rat Astrocytes.Neurochemical research · 2025Article
- Proline Metabolism in Cancer: Emerging Roles in Redox Homeostasis and Therapeutic Opportunities.Cancers · 2025Review
- Multifunctionality and Possible Medical Application of the BPC 157 Peptide-Literature and Patent Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Metabolic Reprogramming at the Edge of Redox: Connections Between Metabolic Reprogramming and Cancer Redox State.International journal of molecular sciences · 2025Review
- L-Proline Alters Energy Metabolism in Brain Cortical Tissue Slices.Neurochemical research · 2024Article
- Cysteamine dioxygenase (ADO) governs cancer cell mitochondrial redox homeostasis through proline metabolism.Science advances · 2024Article
- Proteo-metabolomics and patient tumor slice experiments point to amino acid centrality for rewired mitochondria in fibrolamellar carcinoma.Cell reports. Medicine · 2024Article
- The nonphototrophic hypocotyl 3 (NPH3) domain protein NRL5 is a trafficking-associated GTPase essential for drought resistance.Science advances · 2024Article
- Deubiquitinase USP9x regulates the proline biosynthesis pathway in non-small cell lung cancer.Cell death discovery · 2024Article
- Single Amino Acids as Sole Nitrogen Source for the Production of Lipids and Coenzyme Q byMicroorganisms · 2024Article
- Identification ofTranslational cancer research · 2024Article
- PRODH safeguards human naive pluripotency by limiting mitochondrial oxidative phosphorylation and reactive oxygen species production.EMBO reports · 2024Article
- Please, carefully, pass the P5C.Journal of experimental botany · 2024Article
- Article
- Proline catabolism is a key factor facilitating Candida albicans pathogenicity.PLoS pathogens · 2023Article
- Loss of attachment promotes proline accumulation and excretion in cancer cells.Science advances · 2023Article
- Discovery of long non-coding RNAs in Aspergillus flavus response to water activity, COScientific reports · 2023Article
- Can proline dehydrogenase-a key enzyme involved in proline metabolism-be a novel target for cancer therapy?Frontiers in oncology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
Proline dehydrogenase/oxidase (PRODH/POX) is a mitochondrial protein critical to multiple stress pathways. Because of the roles of PRODH/POX in signaling, and its shared localization to the mitochondrial inner membrane with the electron transport chain (ETC), we investigated whether there was a direct relationship between PRODH/POX and regulation of the ETC. We found that PRODH/POX binds directly to CoQ1 and that CoQ1-dependent PRODH/POX activity required functional Complex III and Complex IV. PRODH/POX supported respiration in living cells during nutrient stress; however, expression of PRODH/POX resulted in an overall decrease in respiratory fitness. Effects on respiratory fitness were inhibited by DHP and NAC, indicating that these effects were mediated by PRODH/POX-dependent reactive oxygen species (ROS) generation. PRODH/POX expression resulted in a dose-dependent down-regulation of Complexes I-IV of the ETC, and this effect was also mitigated by the addition of DHP and NAC. We found that succinate was an uncompetitive inhibitor of PRODH/POX activity, inhibited ROS generation by PRODH/POX, and alleviated PRODH/POX effects on respiratory fitness. The findings demonstrate novel cross-talk between proline and succinate respiration in vivo and provide mechanistic insights into observations from previous animal studies. Our results suggest a potential regulatory loop between PRODH/POX and succinate in regulation of mitochondrial respiration.
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