ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
A role for FE65 in controlling GnRH-1 neurogenesis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Loss of the endoplasmic reticulum protein canopy 1 disrupts the function and circuit organization of V2R-expressing vomeronasal sensory neurons.Development (Cambridge, England) · 2026Article
- Haploinsufficiency of Sox2 causes fewer GnRH neurons and delayed puberty in mice.Endocrinology · 2026Article
- De novo rare EMX2 variants lead to idiopathic hypogonadotropic hypogonadism.Genetics in medicine : official journal of the American College of Medical Genetics · 2026Article
- Tracing Early Migratory Neurons in the Developing Nose Using Contactin-2 (Cntn2) CreERT2.Genesis (New York, N.Y. : 2000) · 2025Article
- Essential Regulation of Spermatogonial Stem Cell Fate Decisions and Male Fertility by APBB1 via Interaction with KAT5 and GDF15 in Humans and Mice.Research (Washington, D.C.) · 2025Article
- Mild Gestational Hypothyroidism in Mice Has Transient Developmental Effects and Long-Term Consequences on Neuroendocrine Systems.Thyroid : official journal of the American Thyroid Association · 2025Article
- FE65: a hub for neurodevelopment.Neural regeneration research · 2024Article
- Article
- Mechanisms underlying pre- and postnatal development of the vomeronasal organ.Cellular and molecular life sciences : CMLS · 2021Review
- Characterization of the human GnRH neuron developmental transcriptome using aDisease models & mechanisms · 2020Article
- Gli3 Regulates Vomeronasal Neurogenesis, Olfactory Ensheathing Cell Formation, and GnRH-1 Neuronal Migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Identifying Isl1 Genetic Lineage in the Developing Olfactory System and in GnRH-1 Neurons.Frontiers in physiology · 2020Article
- Medication for Acromegaly Reduces Expression of MUC16, MACC1 and GRHL2 in Pituitary Neuroendocrine Tumour Tissue.Frontiers in oncology · 2020Article
- GnRH-1 Neural Migration From the Nose to the Brain Is Independent From Slit2, Robo3 and NELL2 Signaling.Frontiers in cellular neuroscience · 2019Article
- GnRH-(1-5) Inhibits TGF-β Signaling to Regulate the Migration of Immortalized Gonadotropin-Releasing Hormone Neurons.Frontiers in endocrinology · 2018Article
- Fe65 Suppresses Breast Cancer Cell Migration and Invasion through Tip60 Mediated Cortactin Acetylation.Scientific reports · 2015Article
- FE65 and FE65L1 amyloid precursor protein-binding protein compound null mice display adult-onset cataract and muscle weakness.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- GnRH, anosmia and hypogonadotropic hypogonadism--where are we?Frontiers in neuroendocrinology · 2015Review
- The indirect role of fibroblast growth factor-8 in defining neurogenic niches of the olfactory/GnRH systems.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Discovery of single nucleotide polymorphisms in candidate genes associated with fertility and production traits in Holstein cattle.BMC genetics · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Gonadotropin-releasing hormone-1 (GnRH-1) neurons migrate from the nasal placode to the forebrain where they control gonadal function via the hypothalamic-pituitary-gonadal axis. The birth of GnRH-1-expressing neurons is one of the first neurogenic events in the developing nasal placode. By gene expression screening on single GnRH-1 neurons, amyloid precursor binding protein-1 (FE65) was identified in migratory GnRH-1 neurons. FE65 has been shown to modulate β1-integrin dynamics, actin cytoskeleton, cell motility, and FE65/amyloid precursor protein signaling has been described in neuro/glial cell fate determination as well as in modulating neurogenesis. Analysis of two mouse lines, one deficient for the 97 kDa FE65 isoform and a second deficient for the 97 and 60 kDa forms of FE65, showed overlapping phenotypes. In both lines, no migratory defects of the GnRH-1 neurons were observed, but a 25% increase in GnRH-1 neuronal number during embryonic development was found. Bromodeoxyuridine birth tracing and spatiotemporal tracking of GnRH-1 cell precursors demonstrated that the lack of the N-terminal portion of FE65, which includes part of the functional nuclear translocation/gene transcription domain of FE65 (WW domain), extends the timing of GnRH-1 neurogenesis in the developing nasal placode without affecting proliferation of GnRH-1 neuronal progenitors or cell death. The observed changes in the dynamics of GnRH-1 neurogenesis highlight a unique role for the 97 kDa isoform of FE65 and suggest that GnRH-1 cells, which have a short neurogenic window, originate from multipotent progenitors able to generate distinct cell types as GnRH-1 neurogenesis declines in response to environmental changes.
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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.