ReviewMolecular endocrinology (Baltimore, Md.)2015
Minireview: Activin Signaling in Gonadotropes: What Does the FOX say… to the SMAD?
Review in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
31 citing papers in PubMed, 53 citations in OpenAlex.
- Discovery proteomics identification of factors contributing to gonadotropin β expression.Endocrinology · 2026Article
- Screening and Preliminary Identification of Inhibin α Subunit-Specific Nanobodies Through High-Throughput Sequencing Combined with Mass Spectrometry.Animals : an open access journal from MDPI · 2026Article
- Regulation of murine follicle-stimulating hormone β subunit transcription by newly identified enhancers.Endocrinology · 2026Article
- Molecular Mechanisms of Dysregulated LH and FSH Secretion in Human Reproductive Failure.Biomedicines · 2026Review
- Regulation of murine follicle-stimulating hormone β subunit transcription by newly identified enhancers.bioRxiv : the preprint server for biology · 2025Article
- Evidence for divergent endocrine regulation of the murine and ovine GnRH receptor gene promoters.Frontiers in endocrinology · 2025Article
- Article
- Follicle-stimulating hormone.Trends in endocrinology and metabolism: TEM · 2024Article
- Steroidogenic Factor 1 Regulates Transcription of the Inhibin B Coreceptor in Pituitary Gonadotrope Cells.Endocrinology · 2022Article
- Pituitary gonadotroph-specific patterns of gene expression and hormone secretion.Current opinion in pharmacology · 2022Review
- Article
- TGFBR3L is an inhibin B co-receptor that regulates female fertility.Science advances · 2021Article
- Enhancing Gonadotrope Gene Expression Through Regulatory lncRNAs.Endocrinology · 2021Review
- Androgen receptor positively regulates gonadotropin-releasing hormone receptor in pituitary gonadotropes.Molecular and cellular endocrinology · 2021Article
- IGSF1 Does Not Regulate Spermatogenesis or Modify FSH Synthesis in Response to Inhibins or Activins.Journal of the Endocrine Society · 2021Article
- Post-Transcriptional Regulation ofInternational journal of molecular sciences · 2021Review
- PACAP: A regulator of mammalian reproductive function.Molecular and cellular endocrinology · 2020Review
- AMP-activated protein kinase activation reduces the transcriptional activity of the murine luteinizing hormone β-subunit gene.The Journal of reproduction and development · 2020Article
- Foxf2 and Smad6 co-regulation of collagen 5A2 transcription is involved in the pathogenesis of intrauterine adhesion.Journal of cellular and molecular medicine · 2020Article
- Commentary on the Recent FSH Collection: Known Knowns and Known Unknowns.Endocrinology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The activins were discovered and named based on their abilities to stimulate FSH secretion and FSHβ (Fshb) subunit expression by pituitary gonadotrope cells. According to subsequent in vitro observations, activins also stimulate the transcription of the GnRH receptor (Gnrhr) and the activin antagonist, follistatin (Fst). Thus, not only do activins stimulate FSH directly, they have the potential to regulate both FSH and LH indirectly by modulating gonadotrope sensitivity to hypothalamic GnRH. Moreover, activins may negatively regulate their own actions by stimulating the production of one of their principal antagonists. Here, we describe our current understanding of the mechanisms through which activins regulate Fshb, Gnrhr, and Fst transcription in vitro. The activin signaling molecules SMAD3 and SMAD4 appear to partner with the winged-helix/forkhead transcription factor, forkhead box L2 (FOXL2), to regulate expression of all 3 genes. However, in vivo data paint a different picture. Although conditional deletion of Foxl2 and/or Smad4 in murine gonadotropes produces impairments in FSH synthesis and secretion as well as in pituitary Fst expression, Gnrhr mRNA levels are either unperturbed or increased in these animals. Surprisingly, gonadotrope-specific deletion of Smad3 alone or with Smad2 does not impair FSH production or fertility; however, mice harboring these mutations may express a DNA binding-deficient, but otherwise functional, SMAD3 protein. Collectively, the available data firmly establish roles for FOXL2 and SMAD4 in Fshb and Fst expression in gonadotrope cells, whereas SMAD3's role requires further investigation. Gnrhr expression, in contrast, appears to be FOXL2, SMAD4, and, perhaps, activin independent in vivo.
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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.