ArticleNature communications2023
SEMA6A drives GnRH neuron-dependent puberty onset by tuning median eminence vascular permeability.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Systematic genotype-phenotype mapping and transcriptomic analyses highlight SEMA6A as a candidate for neuronal migration defects in 5q22-q23 deletions.Journal of human genetics · 2026Article
- Combined HS6ST1 and HS6ST2 loss disrupts the formation and migration of gonadotropin-releasing hormone neurons.Development (Cambridge, England) · 2026Article
- Genome-wide association study identifies toll-like receptor four protein-mediated metabolic remodelling affecting gout pathogenesis.Journal of global health · 2026Observational
- CRISPR activation of DLX5 drives neural progenitors to the GnRH cell fate.Journal of molecular endocrinology · 2026Article
- Recurrent intra-tumour heterogeneity is a hallmark of metastatic prostate cancer.Nature communications · 2026Article
- Hypothalamic control of puberty: from neuronal circuits to mechanisms for its metabolic regulation.Reviews in endocrine & metabolic disorders · 2026Review
- Neuropilin 1 (NRP1) conveys SEMA3A signals to restrict physiological angiogenesis.Angiogenesis · 2026Article
- Nanoplastics Impair GnRH Neuron Migration and Neuroendocrine Function: Emerging Players in the Pathogenesis of Reproductive Disorders.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- NGF administration is associated with increased GnRH immunoreactivity and a GnRH-associated phenotype in hypothalamic NSCs of aging mice.Frontiers in endocrinology · 2026Article
- Neurotrophic Control of Puberty: From Molecular Signaling to Disorders of Pubertal Timing.Current issues in molecular biology · 2025Review
- Identification of Neurotrophic Factor Related Biomarkers and Mechanistic Insights into Neuropathic Pain via Integrated Bioinformatics Analysis.ACS omega · 2025Article
- Proteomic analysis of cerebrospinal fluid from females with multiple sclerosis highlights elevated microglial function and impaired neurogenesis.IBRO neuroscience reports · 2025Article
- Glucose-dependent insulinotropic polypeptide receptor signaling in oligodendrocytes increases the weight-loss action of GLP-1R agonism.Cell metabolism · 2025Article
- Hippo-vgll3 signaling may contribute to sex differences in Atlantic salmon maturation age via contrasting adipose dynamics.Biology of sex differences · 2025Article
- Age, sex, and cell type-resolved hypothalamic gene expression across the pubertal transition in mice.Biology of sex differences · 2024Article
- Methylome analysis in girls with idiopathic central precocious puberty.Clinical epigenetics · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 4 countries.
Funding
Abstract
Innervation of the hypothalamic median eminence by Gonadotropin-Releasing Hormone (GnRH) neurons is vital to ensure puberty onset and successful reproduction. However, the molecular and cellular mechanisms underlying median eminence development and pubertal timing are incompletely understood. Here we show that Semaphorin-6A is strongly expressed by median eminence-resident oligodendrocytes positioned adjacent to GnRH neuron projections and fenestrated capillaries, and that Semaphorin-6A is required for GnRH neuron innervation and puberty onset. In vitro and in vivo experiments reveal an unexpected function for Semaphorin-6A, via its receptor Plexin-A2, in the control of median eminence vascular permeability to maintain neuroendocrine homeostasis. To support the significance of these findings in humans, we identify patients with delayed puberty carrying a novel pathogenic variant of SEMA6A. In all, our data reveal a role for Semaphorin-6A in regulating GnRH neuron patterning by tuning the median eminence vascular barrier and thereby controlling puberty onset.
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What Socratic holds
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 Socratic graph.