ArticleThe Journal of clinical investigation2007
FKBP52 deficiency-conferred uterine progesterone resistance is genetic background and pregnancy stage specific.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed.
- SAV1 in Cooperation With FKBP52 Participates in Implantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- HBP1 enhances progesterone receptor activity and IGFBP1 expression driving endometrial decidualization.Communications biology · 2026Article
- Single-cell transcriptomic atlas of different endometriosis indicating that an interaction between endometriosis-associated mesothelial cells (EAMCs) and ectopic stromal cells may influence progesterone resistance.Clinical and translational medicine · 2025Article
- Unraveling the Dynamics of Estrogen and Progesterone Signaling in the Endometrium: An Overview.Cells · 2024Review
- Stromal Pbrm1 mediates chromatin remodeling necessary for embryo implantation in the mouse uterus.The Journal of clinical investigation · 2024Article
- DCAF2 is essential for the development of uterine epithelia and mouse fertility.Frontiers in cell and developmental biology · 2024Article
- Glucocorticoids, their uses, sexual dimorphisms, and diseases: new concepts, mechanisms, and discoveries.Physiological reviews · 2024Review
- Transgenic mice applications in the study of endometriosis pathogenesis.Frontiers in cell and developmental biology · 2024Review
- Impact of FKBP52 on cell proliferation and hormone-dependent cancers.Cancer science · 2023Review
- MicroRNAs emerging coordinate with placental mammals alter pathways in endometrial epithelia important for endometrial function.iScience · 2023Article
- Uterine epithelial Gp130 orchestrates hormone response and epithelial remodeling for successful embryo attachment in mice.Scientific reports · 2023Article
- Cysteine dioxygenase and taurine are essential for embryo implantation by involving in EJournal of animal science and biotechnology · 2023Article
- P38α MAPK is a gatekeeper of uterine progesterone responsiveness at peri-implantation via Ube3c-mediated PGR degradation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Uterine Deletion ofInternational journal of molecular sciences · 2022Article
- Review
- [miR-483-5p aggravates cisplatin-induced premature ovarian insufficiency in rats by targeting FKBP4].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- The Influence Mechanism of Abnormal Immunophilin FKBP52 on the Expression Levels of PR-A and PR-B in Endometriosis Based on Endometrial Stromal Cell Model in Vitro.Organogenesis · 2021Article
- Retinoblastoma protein promotes uterine epithelial cell cycle arrest and necroptosis for embryo invasion.EMBO reports · 2021Article
- Vitamin D Supplementation Improves Uterine Receptivity in a Rat Model of Vitamin D Deficiency: A Possible Role of HOXA-10/FKBP52 Axis.Frontiers in physiology · 2021Article
- Sex-Steroid Signaling in Lung Diseases and Inflammation.Advances in experimental medicine and biology · 2021Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Immunophilin FKBP52 serves as a cochaperone to govern normal progesterone (P(4)) receptor (PR) function. Using Fkbp52(-/-) mice, we show intriguing aspects of uterine P(4)/PR signaling during pregnancy. Implantation failure is the major phenotype found in these null females, which is conserved on both C57BL6/129 and CD1 backgrounds. However, P(4) supplementation rescued implantation and subsequent decidualization in CD1, but not C57BL6/129, null females. Surprisingly, experimentally induced decidualization in the absence of blastocysts failed in Fkbp52(-/-) mice on either background even with P(4) supplementation, suggesting that embryonic signals complement uterine signaling for this event. Another interesting finding was that while P(4) at higher than normal pregnancy levels conferred PR signaling sufficient for implantation in CD1 null females, these levels were inefficient in maintaining pregnancy to full term. However, elevating P(4) levels further restored PR signaling to a level optimal for successful term pregnancy with normal litter size. Collectively, the results show that the indispensability of FKBP52 in uterine P(4)/PR signaling is a function of genetic disparity and is pregnancy stage specific. Since there is evidence for a correlation between P(4) supplementation and reduced risks of P(4)-resistant recurrent miscarriages and remission of endometriosis, these findings have clinical implications for genetically diverse populations of women.
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