ArticleProceedings of the National Academy of Sciences of the United States of America2022
Inefficient development of syncytiotrophoblasts in the
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
The trial behind it
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- DHODH regulates trophoblast fusion via IFITM-reduced plasma membrane fluidity: Implications for hypertensive disorders of pregnancy.iScience · 2026Article
- Maternal Melatonin Supplementation Modulates Placental DNA Methylation and Gene Expression in Nutrient-Restricted Cattle.International journal of molecular sciences · 2025Article
- Insight Into Body Size Evolution in Aves: Based on Some Body Size-Related Genes.Integrative zoology · 2025Article
- Human Decidual RUNX1 Promotes Angiogenesis and Trophoblast Differentiation by Regulating Extracellular Vesicle Signaling.Endocrinology · 2025Article
- The P4-phospholipid flippase Atp11a is required for maintenance of eye and ear structure in zebrafish.Journal of cell science · 2025Article
- Phospholipid flippase ATP11A brokers uterine epithelial integrity and function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Trophoblast Fusion in Hypertensive Disorders of Pregnancy and Preeclampsia.International journal of molecular sciences · 2025Review
- Dys-regulated phosphatidylserine externalization as a cell intrinsic immune escape mechanism in cancer.Cell communication and signaling : CCS · 2025Review
- Substrates, regulation, cellular functions, and disease associations of P4-ATPases.Communications biology · 2025Review
- Genetic and Environmental Contributors To Congenital Heart Disease.Current treatment options in cardiovascular medicine · 2025Review
- Dynamic intrauterine crosstalk promotes porcine embryo implantation during early pregnancy.Science China. Life sciences · 2024Article
- Flipping the script: Advances in understanding how and why P4-ATPases flip lipid across membranes.Biochimica et biophysica acta. Molecular cell research · 2024Review
- PIBF1 regulates trophoblast syncytialization and promotes cardiovascular development.Nature communications · 2024Article
- Inhibition of miR-4763-3p expression activates the PI3K/mTOR/Bcl2 autophagy signaling pathway to ameliorate cognitive decline.International journal of biological sciences · 2024Article
- ATP11A Promotes Epithelial-mesenchymal Transition in Gastric Cancer Cells via the Hippo Pathway.Journal of Cancer · 2024Article
- Direct androgen receptor control of sexually dimorphic gene expression in the mammalian kidney.Developmental cell · 2023Article
- Trophoblast Differentiation: Mechanisms and Implications for Pregnancy Complications.Nutrients · 2023Review
- Regulation of phospholipid distribution in the lipid bilayer by flippases and scramblases.Nature reviews. Molecular cell biology · 2023Review
- Direct androgen receptor regulation of sexually dimorphic gene expression in the mammalian kidney.bioRxiv : the preprint server for biology · 2023Article
- Defects in placental syncytiotrophoblast cells are a common cause of developmental heart disease.Nature communications · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The P4-ATPases ATP11A and ATP11C function as flippases at the plasma membrane to translocate phosphatidylserine from the outer to the inner leaflet. We herein demonstrated that Atp11a-deficient mouse embryos died at approximately E14.5 with thin-walled heart ventricles. However, the cardiomyocyte- or epiblast-specific Atp11a deletion did not affect mouse development or mortality. ATP11C may have compensated for the function of ATP11A in most of the cell types in the embryo. On the other hand, Atp11a, but not Atp11c, was expressed in the mouse placenta, and the Atp11a-null mutation caused poor development of the labyrinthine layer with an increased number of TUNEL-positive foci. Immunohistochemistry and electron microscopy revealed a disorganized labyrinthine layer with unfused trophoblasts in the Atp11a-null placenta. Human placenta-derived choriocarcinoma BeWo cells expressed the ATP11A and ATP11C genes. A lack of ATP11A and ATP11C eliminated the ability of BeWo cells to flip phosphatidylserine and fuse when treated with forskolin. These results indicate that flippases at the plasma membrane play an important role in the formation of syncytiotrophoblasts in placental development.
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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.