ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Follicle-stimulating hormone synthesis and fertility are intact in mice lacking SMAD3 DNA binding activity and SMAD2 in gonadotrope cells.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- A Point Mutation in an Otherwise Dispensable Upstream Fshb Enhancer Moderately Impairs Fertility in Female Mice.Endocrinology · 2025Article
- Revisiting the gonadotropic regulation of mammalian spermatogenesis: evolving lessons during the past decade.Frontiers in endocrinology · 2023Review
- The Hippo Pathway Effectors YAP and TAZ Regulate LH Release by Pituitary Gonadotrope Cells in Mice.Endocrinology · 2022Article
- Development of a Highly Sensitive ELISA for Measurement of FSH in Serum, Plasma, and Whole Blood in Mice.Endocrinology · 2021Article
- The Therapeutic Effect of Stem Cells on Chemotherapy-Induced Premature Ovarian Failure.Current molecular medicine · 2021Review
- Betaglycan (TGFBR3) Functions as an Inhibin A, but Not Inhibin B, Coreceptor in Pituitary Gonadotrope Cells in Mice.Endocrinology · 2018Article
- Exosomes derived from human adipose mesenchymal stem cells improve ovary function of premature ovarian insufficiency by targeting SMAD.Stem cell research & therapy · 2018Article
- Regulation of reproduction via tight control of gonadotropin hormone levels.Molecular and cellular endocrinology · 2018Review
- GnRH Receptor Expression and Reproductive Function Depend on JUN in GnRH Receptor‒Expressing Cells.Endocrinology · 2018Article
- Sex- and Age-Specific Impact of ERK Loss Within the Pituitary Gonadotrope in Mice.Endocrinology · 2018Article
- The TGF-β Family in the Reproductive Tract.Cold Spring Harbor perspectives in biology · 2017Review
- SMAD3 Regulates Follicle-stimulating Hormone Synthesis by Pituitary Gonadotrope CellsThe Journal of biological chemistry · 2017Article
- Leptin Regulation of Gonadotrope Gonadotropin-Releasing Hormone Receptors As a Metabolic Checkpoint and Gateway to Reproductive Competence.Frontiers in endocrinology · 2017Article
- Characterization of Gonadotrope Secretoproteome Identifies Neurosecretory Protein VGF-derived Peptide Suppression of Follicle-stimulating Hormone Gene Expression.The Journal of biological chemistry · 2016Article
- GnRH Pulse Frequency Control of Fshb Gene Expression Is Mediated via ERK1/2 Regulation of ICER.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Minireview: Activin Signaling in Gonadotropes: What Does the FOX say… to the SMAD?Molecular endocrinology (Baltimore, Md.) · 2015Review
- β-catenin stabilization in gonadotropes impairs FSH synthesis in male mice in vivo.Endocrinology · 2015Article
- Follicle-stimulating hormone synthesis and fertility depend on SMAD4 and FOXL2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
The activin/inhibin system regulates follicle-stimulating hormone (FSH) synthesis and release by pituitary gonadotrope cells in mammals. In vitro cell line data suggest that activins stimulate FSH β-subunit (Fshb) transcription via complexes containing the receptor-regulated SMAD proteins SMAD2 and SMAD3. Here, we used a Cre-loxP approach to determine the necessity for SMAD2 and/or SMAD3 in FSH synthesis in vivo. Surprisingly, mice with conditional mutations in both Smad2 and Smad3 specifically in gonadotrope cells are fertile and produce FSH at quantitatively normal levels. Notably, however, we discovered that the recombined Smad3 allele produces a transcript that encodes the entirety of the SMAD3 C-terminal Mad homology 2 (MH2) domain. This protein behaves similarly to full-length SMAD3 in Fshb transcriptional assays. As the truncated protein lacks the N-terminal Mad homology 1 (MH1) domain, these results show that SMAD3 DNA-binding activity as well as SMAD2 are dispensable for normal FSH synthesis in vivo. Furthermore, the observation that deletion of proximal exons does not remove all SMAD3 function may facilitate interpretation of divergent phenotypes previously described in different Smad3 knockout mouse lines.
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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.