ArticleJournal of molecular medicine (Berlin, Germany)2019
IDH-1 deficiency induces growth defects and metabolic alterations in GSPD-1-deficient Caenorhabditis elegans.
Article in Journal of molecular medicine (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Analysis of the interlink between glucose-6-phosphate dehydrogenase (G6PD) and lung cancer through multi-omics databases.Heliyon · 2024Article
- The acetylation of MDH1 and IDH1 is associated with energy metabolism in acute liver failure.iScience · 2024Article
- Genome-wide association analysis explores the genetic loci of amino acid content in duck's breast muscle.BMC genomics · 2024Article
- Transcriptome Analysis Reveals the Molecular Mechanisms Underlying Growth Superiority in a NovelGenes · 2024Article
- Computational Approaches for Identification of Potential Plant Bioactives as Novel G6PD Inhibitors Using Advanced Tools and Databases.Molecules (Basel, Switzerland) · 2023Article
- Differential regulation of degradation and immune pathways underlies adaptation of the ectosymbiotic nematode Laxus oneistus to oxic-anoxic interfaces.Scientific reports · 2022Article
- G6PD upregulates Cyclin E1 and MMP9 to promote clear cell renal cell carcinoma progression.International journal of medical sciences · 2022Article
- Relationship of Carbohydrate Metabolism and Molecular Genetic Markers in Gliomas with Different Degree of Anaplasia.Bulletin of experimental biology and medicine · 2021Article
- G6PD: A hub for metabolic reprogramming and redox signaling in cancer.Biomedical journal · 2021Review
- Quo VadisMetabolites · 2021Review
- G6PD deficiency, redox homeostasis, and viral infections: implications for SARS-CoV-2 (COVID-19).Free radical research · 2021Review
- Modeling human glucose-6-phosphate dehydrogenase mutations usingmicroPublication biology · 2021Article
- Article
- Review
- Neonicotinoid-containing insecticide disruption of growth, locomotion, and fertility in Caenorhabditis elegans.PloS one · 2020Article
- Review
- Cytoplasmic and Mitochondrial NADPH-Coupled Redox Systems in the Regulation of Aging.Nutrients · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NADPH is a reducing equivalent that maintains redox homeostasis and supports reductive biosynthesis. Lack of major NADPH-producing enzymes predisposes cells to growth retardation and demise. It was hypothesized that double deficiency of the NADPH-generating enzymes, GSPD-1 (Glucose-6-phosphate 1-dehydrogenase), a functional homolog of human glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway, and IDH-1 (isocitrate dehydrogenase-1) affect growth and development in the nematode, Caenorhabditis elegans (C. elegans). The idh-1;gspd-1(RNAi) double-deficient C. elegans model displayed shrinkage of body size, growth retardation, slowed locomotion, and impaired molting. Global metabolomic analysis was employed to address whether or not metabolic pathways were altered by severe NADPH insufficiency by the idh-1;gspd-1(RNAi) double-deficiency. The principal component analysis (PCA) points to a distinct metabolomic profile of idh-1;gspd-1(RNAi) double-deficiency. Further metabolomic analysis revealed that NADPH-dependent and glutamate-dependent amino acid biosynthesis were significantly affected. The reduced pool of amino acids may affect protein synthesis, as indicated by the absence of NAS-37 expression during the molting process. In short, double deficiency of GSPD-1 and IDH-1 causes growth retardation and molting defects, which are, in part, attributed to defective protein synthesis, possibly mediated by altered amino acid biosynthesis and metabolism in C. elegans.
Indexed as
Identifiers
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.