ArticlePNAS nexus2025
Loss of PRICKLE1 leads to abnormal endometrial epithelial architecture, decreased embryo implantation, and reduced fertility in mice.
Article in PNAS nexus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Back to the Future-A 50-Year Dive into Embryo Implantation Research: Cell Biological Paradox, Epithelial Cell Polarity, and EMT.Biomolecules · 2026Review
- HOXA10-TWIST2 antagonism drives partial epithelial-to-mesenchymal transition for embryo implantation.Cell death discovery · 2025Article
- Contrasting Effects of Phosphatidylcholine and Betaine Supplementation on Embryonic Development in a Mouse Model of the MTHFD1 R653Q Variant.The Journal of nutrition · 2025Article
- Loss of PRICKLE1 leads to abnormal endometrial epithelial architecture, decreased embryo implantation, and reduced fertility in mice.PNAS nexus · 2025Article
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6 authors.
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Abstract
Successful embryo implantation requires coordinated changes in the uterine luminal epithelium, including structural adaptations, apical-basal polarity shifts, intrauterine fluid resorption, and cellular communication. Planar cell polarity proteins, essential for cell organization, are understudied in the context of uterine physiology and implantation. PRICKLE proteins, components of PCP, are suggested to play critical roles in epithelial polarization and tissue morphogenesis. However, their function in the polarized unicellular layer of endometrial epithelium, which supports embryo implantation, is unknown. We developed an endometrial epithelial-specific knockout of mouse
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