ArticleFree radical biology & medicine2007
Effects of thioredoxin reductase-1 deletion on embryogenesis and transcriptome.
Article in Free radical biology & medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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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Who cites it
50 citing papers in PubMed, 114 citations in OpenAlex.
- Developmental Regulation of the Murine Selenoproteome Across Embryonic and Postnatal Stages: Implications for Human Nutrition and Health.Nutrients · 2025Article
- Distinct roles for the thioredoxin and glutathione antioxidant systems in Nrf2-Mediated lung tumor initiation and progression.Redox biology · 2025Article
- Navigating redox imbalance: the role of oxidative stress in embryonic development and long-term health outcomes.Frontiers in cell and developmental biology · 2025Review
- Unraveling the genetics of arsenic toxicity with cellular morphology QTL.PLoS genetics · 2024Article
- Insights into the Multifaceted Roles of Thioredoxin-1 System: Exploring Knockout Murine Models.Biology · 2024Review
- Unresolved questions regarding cellular cysteine sources and their possible relationships to ferroptosis.Advances in cancer research · 2024Review
- Cell morphology QTL reveal gene by environment interactions in a genetically diverse cell population.bioRxiv : the preprint server for biology · 2023Article
- Selenium in Prostate Cancer: Prevention, Progression, and Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
- NRF2 and the Moirai: Life and Death Decisions on Cell Fates.Antioxidants & redox signaling · 2023Review
- Selenoproteins and the senescence-associated epitranscriptome.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Thioredoxin Reductase 1 Modulates Pigmentation and Photobiology of Murine Melanocytes in vivo.The Journal of investigative dermatology · 2022Article
- Neddylation Inhibition Causes Impaired Mouse Embryo Quality and Blastocyst Hatching Failure Through Elevated Oxidative Stress and Reduced IL-1β.Frontiers in immunology · 2022Article
- Deletion of Thioredoxin Reductase Disrupts Redox Homeostasis and Impairs β-Cell Function.Function (Oxford, England) · 2022Article
- Supplemental Ascorbate Diminishes DNA Damage Yet Depletes Glutathione and Increases Acute Liver Failure in a Mouse Model of Hepatic Antioxidant System Disruption.Antioxidants (Basel, Switzerland) · 2021Article
- Mitochondrial CaJournal of molecular and cellular cardiology · 2021Review
- Effects of Mammalian Thioredoxin Reductase Inhibitors.Handbook of experimental pharmacology · 2021Article
- The epitranscriptomic writer ALKBH8 drives tolerance and protects mouse lungs from the environmental pollutant naphthalene.Epigenetics · 2020Article
- Carbonyl Reductase 1 Plays a Significant Role in Converting Doxorubicin to Cardiotoxic Doxorubicinol in Mouse Liver, but the Majority of the Doxorubicinol-Forming Activity Remains Unidentified.Drug metabolism and disposition: the biological fate of chemicals · 2020Article
- Epitranscriptomic systems regulate the translation of reactive oxygen species detoxifying and disease linked selenoproteins.Free radical biology & medicine · 2019Review
- Selenium, Selenoproteins, and Female Reproduction: A Review.Molecules (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Thioredoxin reductases (Txnrd) maintain intracellular redox homeostasis in most organisms. Metazoan Txnrds also participate in signal transduction. Mouse embryos homozygous for a targeted null mutation of the txnrd1 gene, encoding the cytosolic thioredoxin reductase, were viable at embryonic day 8.5 (E8.5) but not at E9.5. Histology revealed that txnrd1-/- cells were capable of proliferation and differentiation; however, mutant embryos were smaller than wild-type littermates and failed to gastrulate. In situ marker gene analyses indicated that primitive streak mesoderm did not form. Microarray analyses on E7.5 txnrd-/- and txnrd+/+ littermates showed similar mRNA levels for peroxiredoxins, glutathione reductases, mitochondrial Txnrd2, and most markers of cell proliferation. Conversely, mRNAs encoding sulfiredoxin, IGF-binding protein 1, carbonyl reductase 3, glutamate cysteine ligase, glutathione S-transferases, and metallothioneins were more abundant in mutants. Many gene expression responses mirrored those in thioredoxin reductase 1-null yeast; however, mice exhibited a novel response within the peroxiredoxin catalytic cycle. Thus, whereas yeast induce peroxiredoxin mRNAs in response to thioredoxin reductase disruption, mice induced sulfiredoxin mRNA. In summary, Txnrd1 was required for correct patterning of the early embryo and progression to later development. Conserved responses to Txnrd1 disruption likely allowed proliferation and limited differentiation of the mutant embryo cells.
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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.