ArticleThe EMBO journal2002
Maternally transmitted severe glucose 6-phosphate dehydrogenase deficiency is an embryonic lethal.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 3 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
69 citing papers in PubMed, 3 syntheses or guidelines pooled it, 157 citations in OpenAlex.
- Epidemiology of glucose-6-phosphate dehydrogenase deficiency in 10 malaria-endemic countries in sub-Saharan Africa: a systematic review.The Pan African medical journal · 2025Pooled it
- Expanded Clinical Pharmacogenetics Implementation Consortium Guideline for Medication Use in the Context of G6PD Genotype.Clinical pharmacology and therapeutics · 2023Guideline
- Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines for rasburicase therapy in the context of G6PD deficiency genotype.Clinical pharmacology and therapeutics · 2014Guideline
- Association between G6PD gene variants and adverse pregnancy outcomes.BMC pregnancy and childbirth · 2026Article
- Integrative Multi-Omics Analysis Unveils Biomarkers Linking the Gut Microbiota, Blood Metabolites, and Recurrent Pregnancy Loss.International journal of women's health · 2026Article
- Insights into Neutrophil Dysfunction in Inherited Metabolic Disorders.Journal of innate immunity · 2026Review
- G6PD deficiency as a underrecognized genetic risk factor for rare neurological disorders: evidence from a population-based genetic analysis.Frontiers in genetics · 2026Article
- Effects of aging and anti-aging dietary restriction on regulators of the [NADPH]/[NADPFree radical biology & medicine · 2025Review
- Spatial Partitioning of Core Glycolysis Enables Tissue-Specific Metabolic Programs In Vivo.bioRxiv : the preprint server for biology · 2025Article
- Review
- Navigating redox imbalance: the role of oxidative stress in embryonic development and long-term health outcomes.Frontiers in cell and developmental biology · 2025Review
- Analysis of the interlink between glucose-6-phosphate dehydrogenase (G6PD) and lung cancer through multi-omics databases.Heliyon · 2024Article
- Review
- Analysis of the Effects of Pentose Phosphate Pathway Inhibition on the Generation of Reactive Oxygen Species and Epileptiform Activity in Hippocampal Slices.International journal of molecular sciences · 2024Article
- The pentose phosphate pathway in health and disease.Nature metabolism · 2023Review
- Remove, Refine, Reduce: Cell Death in Biological Systems.International journal of molecular sciences · 2023Article
- G6PDH as a key immunometabolic and redox trigger in arthropods.Frontiers in physiology · 2023Review
- Glucose 6 phosphatase dehydrogenase (G6PD): a novel diagnosis marker related to gastrointestinal cancers.American journal of translational research · 2023Article
- Review
- Glucose-6-Phosphate Dehydrogenase, Redox Homeostasis and Embryogenesis.International journal of molecular sciences · 2022Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Mouse chimeras from embryonic stem cells in which the X-linked glucose 6-phosphate dehydrogenase (G6PD) gene had been targeted were crossed with normal females. First-generation (F(1)) G6PD(+/-) heterozygotes born from this cross were essentially normal; analysis of their tissues demonstrated strong selection for cells with the targeted G6PD allele on the inactive X chromosome. When these F(1) G6PD(+/-) females were bred to normal males, only normal G6PD mice were born, because: (i) hemizygous G6PD(-) male embryos died by E10.5 and their development was arrested from E7.5, the time of onset of blood circulation; (ii) heterozygous G6PD(+/-) females showed abnormalities from E8.5, and died by E11.5; and (iii) severe pathological changes were present in the placenta of both G6PD(-) and G6PD(+/-) embryos. Thus, G6PD is not indispensable for early embryo development; however, severe G6PD deficiency in the extraembryonic tissues (consequent on selective inactivation of the normal paternal G6PD allele) impairs the development of the placenta and causes death of the embryo. Most importantly, G6PD is indispensable for survival when the embryo is exposed to oxygen through its blood supply.
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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.