ArticleBiochemical and biophysical research communications2015
Mig-6 regulates endometrial genes involved in cell cycle and progesterone signaling.
Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- MIG-6 Plays a Critical Role as a PGR Mediator in Maintaining Epithelial and Stromal Cells for Uterine Receptivity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Review
- Cited2 is a key regulator of placental development and plasticity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Loss of MIG-6 results in endometrial progesterone resistance via ERBB2.Nature communications · 2022Article
- Review
- Research Progress on the Mechanism Between Polycystic Ovary Syndrome and Abnormal Endometrium.Frontiers in physiology · 2021Review
- Progesterone and Estrogen Signaling in the Endometrium: What Goes Wrong in Endometriosis?International journal of molecular sciences · 2019Review
- Progesterone Resistance in Endometriosis Is Modulated by the Altered Expression of MicroRNA-29c and FKBP4.The Journal of clinical endocrinology and metabolism · 2017Article
- CITED2 modulation of trophoblast cell differentiation: insights from global transcriptome analysis.Reproduction (Cambridge, England) · 2016Article
- Replication of Epigenetic Postpartum Depression Biomarkers and Variation with Hormone Levels.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- LKB1 loss promotes endometrial cancer progression via CCL2-dependent macrophage recruitment.The Journal of clinical investigation · 2015Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Mitogen inducible gene 6 (Mig-6) is an important mediator of progesterone (P4) signaling to inhibit estrogen (E2) signaling in the uterus. Ablation of Mig-6 in the murine uterus leads to the development of endometrial hyperplasia and E2-induced endometrial cancer. To identify the molecular pathways regulated by Mig-6, we performed microarray analysis on the uterus of ovariectomized Mig-6(f/f) and PGR(cre/+)Mig-6(f/f) (Mig-6(d/d)) mice treated with vehicle or P4 for 6 h. The results revealed that 772 transcripts were significantly regulated in the Mig-6(d/d) uterus treated with vehicle as compared with Mig-6(f/f) mice. The pathway analysis showed that Mig-6 suppressed the expression of gene-related cell cycle regulation in the absence of ovarian steroid hormone. The epithelium of Mig-6(d/d) mice showed a significant increase in the number of proliferative cells compared to Mig-6(f/f) mice. This microarray analysis also revealed that 324 genes are regulated by P4 as well as Mig-6. Cited2, the developmentally important transcription factor, was identified as being regulated by the P4-Mig-6 axis. To determine the role of Cited2 in the uterus, we used the mice with Cited2 that were conditionally ablated in progesterone receptor-positive cells (PGR(cre/+)Cited2(f/f); Cited2(d/d)). Ablation of Cited2 in the uterus resulted in a significant reduction in the ability of the uterus to undergo a hormonally induced decidual reaction. Identification and analysis of these responsive genes will help define the role of P4 as well as Mig-6 in regulating uterine biology.
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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.