ArticleMolecular endocrinology (Baltimore, Md.)2011
Deletion of Otx2 in GnRH neurons results in a mouse model of hypogonadotropic hypogonadism.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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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
32 citing papers in PubMed, 49 citations in OpenAlex.
- GnRH and Cognition.Endocrinology · 2025Review
- Diagnostic implications of pitfalls in causal variant identification based on 4577 molecularly characterized families.Nature communications · 2023Article
- Autism-linked NLGN3 is a key regulator of gonadotropin-releasing hormone deficiency.Disease models & mechanisms · 2023Article
- Chemogenetic Depletion of Hypophysiotropic GnRH Neurons Does Not Affect Fertility in Mature Female Zebrafish.International journal of molecular sciences · 2022Article
- Development of the gonadotropin-releasing hormone system.Journal of neuroendocrinology · 2022Review
- Article
- Genetics of congenital hypogonadotropic hypogonadism: peculiarities and phenotype of an oligogenic disease.Human genetics · 2021Review
- The Homeodomain Transcription Factors Vax1 and Six6 Are Required for SCN Development and Function.Molecular neurobiology · 2020Article
- Identification of mRNAs and lncRNAs Involved in the Regulation of Follicle Development in Goat.Frontiers in genetics · 2020Article
- Deletion of the Homeodomain Protein Six6 From GnRH Neurons Decreases GnRH Gene Expression, Resulting in Infertility.Endocrinology · 2019Article
- The Contribution of the Circadian GeneJournal of the Endocrine Society · 2019Article
- Haploinsufficiency of Homeodomain Proteins Six3, Vax1, and Otx2 Causes Subfertility in Mice via Distinct Mechanisms.Neuroendocrinology · 2019Review
- Differential CRE Expression in Lhrh-cre and GnRH-cre Alleles and the Impact on Fertility in Otx2-Flox Mice.Neuroendocrinology · 2019Article
- Haploinsufficiency of SIX3 Abolishes Male Reproductive Behavior Through Disrupted Olfactory Development, and Impairs Female Fertility Through Disrupted GnRH Neuron Migration.Molecular neurobiology · 2018Article
- Transcriptional interaction between cFOS and the homeodomain-binding transcription factor VAX1 on the GnRH promoter controls Gnrh1 expression levels in a GnRH neuron maturation specific manner.Molecular and cellular endocrinology · 2018Article
- Genetic risk variants for metabolic traits in Arab populations.Scientific reports · 2017Article
- Kisspeptin Induces Dynamic Chromatin Modifications to Control GnRH Gene Expression.Molecular neurobiology · 2016Article
- Deletion of Vax1 from Gonadotropin-Releasing Hormone (GnRH) Neurons Abolishes GnRH Expression and Leads to Hypogonadism and Infertility.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Genetic variation in total number and locations of GnRH neurons identified using in situ hybridization in a wild-source population.Journal of experimental zoology. Part A, Ecological genetics and physiology · 2016Article
- A small population of hypothalamic neurons govern fertility: the critical role of VAX1 in GnRH neuron development and fertility maintenance.Neuroscience communications · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
GnRH is the central regulator of reproductive function responding to central nervous system cues to control gonadotropin synthesis and secretion. GnRH neurons originate in the olfactory placode and migrate to the forebrain, in which they are found in a scattered distribution. Congenital idiopathic hypogonadotropic hypogonadism (CIHH) has been associated with mutations or deletions in a number of genes that participate in the development of GnRH neurons and expression of GnRH. Despite the critical role of GnRH in mammalian reproduction, a comprehensive understanding of the developmental factors that are responsible for regulating the establishment of mature GnRH neurons and the expression of GnRH is lacking. orthodenticle homeobox 2 (OTX2), a homeodomain protein required for the formation of the forebrain, has been shown to be expressed in GnRH neurons, up-regulated during GnRH neuronal development, and responsible for increased GnRH promoter activity in GnRH neuronal cell lines. Interestingly, mutations in Otx2 have been associated with human hypogonadotropic hypogonadism, but the mechanism by which Otx2 mutations cause CIHH is unknown. Here we show that deletion of Otx2 in GnRH neurons results in a significant decrease in GnRH neurons in the hypothalamus, a delay in pubertal onset, abnormal estrous cyclicity, and infertility. Taken together, these data provide in vivo evidence that Otx2 is critical for GnRH expression and reproductive competence.
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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.