ArticleBiology of reproduction2012
NLRP5 mediates mitochondrial function in mouse oocytes and embryos.
Article in Biology of reproduction, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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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Who cites it
45 citing papers in PubMed, 96 citations in OpenAlex.
- Structure of the mouse cytoplasmic lattice.Nature · 2026Article
- Artificial intelligence-driven high-content imaging decodes for NLRP7-mutant recurrent hydatidiform moles.iScience · 2026Article
- Cellular osmoregulation enhances porcine embryo development by restoring zygotic genome activation via metabolic-epigenetic crosstalk.Cellular & molecular biology letters · 2025Article
- An Nlrp5-null mutation leads to attenuated de novo methylation in oocytes, accompanied by a significant reduction in DNMT3L.Molecular human reproduction · 2025Article
- Two Novel Protein-Truncating Variants in NLRP2 and Their Functional Impacts on the Subcortical Maternal Complex.Clinical genetics · 2025Article
- Effect of genomic regions harboring putative lethal haplotypes on reproductive performance in closed experimental selection lines of Nellore cattle.Scientific reports · 2025Article
- Advances in the genetic etiology of female infertility.Journal of assisted reproduction and genetics · 2024Review
- Cryo-EM structure of the human subcortical maternal complex and the associated discovery of infertility-associated variants.Nature structural & molecular biology · 2024Article
- Single-cell profiling reveals transcriptome dynamics during bovine oocyte growth.BMC genomics · 2024Article
- Single-Cell Transcriptome Analysis Reveals Development-Specific Networks at Distinct Synchronized Antral Follicle Sizes in Sheep Oocytes.International journal of molecular sciences · 2024Article
- Structural basis of the subcortical maternal complex and its implications in reproductive disorders.Nature structural & molecular biology · 2024Article
- Biallelic Recessive Mutations inHuman mutation · 2024Article
- Intracellular fraction of zona pellucida protein 3 is required for the oocyte-to-embryo transition in mice.Molecular human reproduction · 2023Article
- The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023Review
- Inflammasomes as regulators of non-infectious disease.Seminars in immunology · 2023Review
- UHRF1 is essential for proper cytoplasmic architecture and function of mouse oocytes and derived embryos.Life science alliance · 2023Article
- The role of NOD-like receptors in innate immunity.Frontiers in immunology · 2023Review
- DDX1 vesicles control calcium-dependent mitochondrial activity in mouse embryos.Nature communications · 2022Article
- Oocyte aging: looking beyond chromosome segregation errors.Journal of assisted reproduction and genetics · 2022Review
- Posttranslational Regulation of Inflammasomes, Its Potential as Biomarkers and in the Identification of Novel Drugs Targets.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Unraveling molecular pathways responsible for regulation of early embryonic development is crucial for our understanding of female infertility. Maternal determinants that control the transition from oocyte to embryo are crucial molecules that govern developmental competence of the newly conceived zygote. We describe a series of defects that are triggered by a disruption of maternal lethal effect gene, Nlrp5. Previous studies have shown that Nlrp5 hypomorph embryos fail to develop beyond the two-cell stage. Despite its importance in preimplantation development, the mechanism by which the embryo arrest occurs remains unclear. We confirmed that Nlrp5 mutant and wild-type females possess comparable ovarian germ pool and follicular recruitment rates. However, ovulated oocytes lacking Nlrp5 have abnormal mitochondrial localization and increased activity in order to sustain physiological ATP content. This results in an accumulation of reactive oxygen species and increased cellular stress causing mitochondrial depletion. Compromised cellular state is also accompanied by increased expression of cell death inducer Bax and depletion of cytochrome c. However, neither genetic deletion (Bax/Nlrp5 double knockout) nor mimetic interference (BH4 domain or Bax inhibitory peptide) were sufficient to alleviate embryo demise caused by depletion of Nlrp5. We therefore conclude that lack of Nlrp5 in oocytes triggers premature activation of the mitochondrial pool, causing mitochondrial damage that cannot be rescued by inactivation of Bax.
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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.