ArticleBiology of reproduction2017
Med12 regulates ovarian steroidogenesis, uterine development and maternal effects in the mammalian egg.
Article in Biology of reproduction, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Maternal Med12 safeguards trophoblast pluripotency and placental development.Biology of reproduction · 2026Article
- A comprehensive genome-wide analysis for signatures of selection in goat (genus Capra) revealed new candidate genes for environmental adaptation and productive traits.BMC genomics · 2025Article
- The combination of DNA methylome and transcriptome revealed the intergenerational inheritance on the influence of advanced maternal age.Clinical and translational medicine · 2022Article
- Commentary:Frontiers in endocrinology · 2020Article
- Genetics of human female infertility†.Biology of reproduction · 2019Review
- Article
- Expanded Somatic Mutation Spectrum of MED12 Gene in Uterine Leiomyomas of Saudi Arabian Women.Frontiers in genetics · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The transcriptional factor MED12 is part of the essential mediator transcriptional complex that acts as a transcriptional coactivator in all eukaryotes. Missense gain-of-function mutations in human MED12 are associated with uterine leiomyomas, yet the role of MED12 deficiency in tumorigenesis and reproductive biology has not been fully explored. We generated a Med12 reproductive conditional knockout mouse model to evaluate its role in uterine mesenchyme, granulosa cells, and oocytes. Mice heterozygous for Med12 deficiency in granulosa cells and uterus (Med12fl/+ Amhr2-Cre) were subfertile, while mice homozygous for Med12 deficiency in granulosa cells and uterus (Med12fl/fl Amhr2-Cre) were infertile. Morphological and histological analysis of the Med12fl/fl Amhr2-Cre reproductive tract revealed atrophic uteri and hyperchromatic granulosa cells with disrupted expression of Lhcgr, Esr1, and Esr2. Med12fl/fl Amhr2-Cre mice estrous cycle was disrupted, and serum analysis showed blunted rise in estradiol in response to pregnant mare serum gonadotropin. Uterine atrophy was partially rescued by exogenous steroid supplementation with dysregulation of Notch1 and Smo expression in steroid supplemented Med12fl/fl Amhr2-Cre uteri, indicating intrinsic uterine defects. Oocyte-specific ablation of Med12 caused infertility without disrupting normal folliculogenesis and ovulation, consistent with maternal effects of Med12 in early embryo development. These results show the critical importance of Med12 in reproductive tract development and that Med12 loss of function does not cause tumorigenesis in reproductive tissues.
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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.