ArticleEndocrinology2017
How Protein Kinase A Activates Canonical Tyrosine Kinase Signaling Pathways To Promote Granulosa Cell Differentiation.
Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Sex hormone-psoriasis interactions: from sex-specific clinical features to immunoregulatory mechanisms.Frontiers in immunology · 2026Review
- Hypo-glycosylated FSH enhances the ovarian microenvironment for follicular development compared to fully glycosylated FSH.Cell communication and signaling : CCS · 2025Article
- Article
- Protein Kinase A in neurological disorders.Journal of neurodevelopmental disorders · 2024Review
- Oral follicle-stimulating hormone receptor agonist affects granulosa cells differently than recombinant human FSH.Fertility and sterility · 2023Article
- Allethrin Promotes Apoptosis and Autophagy Associated with the Oxidative Stress-Related PI3K/AKT/mTOR Signaling Pathway in Developing Rat Ovaries.International journal of molecular sciences · 2022Article
- The cancer-testis antigen a-kinase anchor protein 3 facilitates breast cancer progression via activation of the PTEN/PI3K/AKT/mTOR signaling.Bioengineered · 2022Article
- Sperm-carried IGF2 downregulated the expression of mitogens produced by Sertoli cells: A paracrine mechanism for regulating spermatogenesis?Frontiers in endocrinology · 2022Article
- Melanocortin-4 receptor and leptin as genes for the selection of superior Madrasin cattle.Veterinary world · 2021Article
- Progesterone affects clinic oocyte yields by coordinating with follicle stimulating hormone via PI3K/AKT and MAPK pathways.Journal of advanced research · 2021Article
- Pseudo-Starvation Driven Energy Expenditure Negatively Affects Ovarian Follicle Development.International journal of molecular sciences · 2021Article
- Profile of follicle-stimulating hormone and polymorphism of follicle-stimulating hormone receptor in Madrasin cattle with ovarian hypofunction.Veterinary world · 2020Article
- Discovery and Preclinical Development of Orally Active Small Molecules that Exhibit Highly Selective Follicle Stimulating Hormone Receptor Agonism.Frontiers in pharmacology · 2020Article
- Dissection of the Ovulatory Process UsingFrontiers in cell and developmental biology · 2020Review
- Commentary on the Recent FSH Collection: Known Knowns and Known Unknowns.Endocrinology · 2020Article
- Effects of Insulin on Porcine Neonatal Sertoli Cell Responsiveness to FSH In Vitro.Journal of clinical medicine · 2019Article
- The IGF1 Receptor Is Involved in Follicle-Stimulating Hormone Signaling in Porcine Neonatal Sertoli Cells.Journal of clinical medicine · 2019Article
- Perturbations in Lineage Specification of Granulosa and Theca Cells May Alter Corpus Luteum Formation and Function.Frontiers in endocrinology · 2019Review
- Molecular Mechanisms of Action of FSH.Frontiers in endocrinology · 2019Review
- Depression promotes prostate cancer invasion and metastasis via a sympathetic-cAMP-FAK signaling pathway.Oncogene · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Protein kinase A (PKA) has recently been shown to mimic the actions of follicle-stimulating hormone (FSH) by activating signaling pathways that promote granulosa cell (GC) differentiation, such as phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK). We sought to elucidate the mechanism by which PKA, a Ser/Thr kinase, intersected the PI3K/AKT and MAPK/ERK pathways that are canonically activated by receptor tyrosine kinases (RTKs). Our results show that for both of these pathways, the RTK is active in the absence of FSH yet signaling down the pathways to commence transcriptional responses requires FSH-stimulated PKA activation. For both pathways, PKA initiates signaling by regulating the activity of a protein phosphatase (PP). For the PI3K/AKT pathway, PKA activates the Ser/Thr PP1 complexed with the insulinlike growth factor 1 receptor (IGF-1R) and insulin receptor substrate 1 (IRS1) to dephosphorylate Ser residues on IRS1, authorizing phosphorylation of IRS1 by the IGF-1R to activate PI3K. Treatment of GCs with FSH and exogenous IGF-1 initiates synergistic IRS1 Tyr phosphorylation and resulting gene activation. The mechanism by which PKA activates PI3K is conserved in preovulatory GCs, MCF7 breast cancer cells, and FRTL thyroid cells. For the MAPK/ERK pathway, PKA promotes inactivation of the MAPK phosphatase (MKP) dual specificity phosphatase (DUSP) MKP3/DUSP6 to permit MEK-phosphorylated ERK to accumulate downstream of the epidermal growth factor receptor. Thus, for the two central signaling pathways that regulate gene expression in GCs, FSH via PKA intersects canonical RTK-regulated signaling by modulating the activity of PPs.
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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.