ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
The gonadotropin-releasing hormone cell-specific element is required for normal puberty and estrous cyclicity.
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 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- The requirement of ubiquitin C-terminal hydrolase L1 in mouse ovarian development and fertility†.Biology of reproduction · 2022Article
- Development of the gonadotropin-releasing hormone system.Journal of neuroendocrinology · 2022Review
- Thimet Oligopeptidase (EC 3.4.24.15) Key Functions Suggested by Knockout Mice Phenotype Characterization.Biomolecules · 2019Article
- Impairments in the reproductive axis of female mice lacking estrogen receptor β in GnRH neurons.American journal of physiology. Endocrinology and metabolism · 2018Article
- Multiple exposures of sevoflurane during pregnancy induces memory impairment in young female offspring mice.Korean journal of anesthesiology · 2017Article
- The Methylcytosine Dioxygenase Ten-Eleven Translocase-2 (tet2) Enables Elevated GnRH Gene Expression and Maintenance of Male Reproductive Function.Endocrinology · 2016Article
- Article
- Insulin receptor signaling in the GnRH neuron plays a role in the abnormal GnRH pulsatility of obese female mice.PloS one · 2015Article
- FBXW12, a novel F box protein-encoding gene, is deleted or methylated in some cases of epithelial ovarian cancer.International journal of clinical and experimental pathology · 2015Article
- Kisspeptin cell-specific PI3K signaling regulates hypothalamic kisspeptin expression and participates in the regulation of female fertility.American journal of physiology. Endocrinology and metabolism · 2014Article
- The regulation of reproductive neuroendocrine function by insulin and insulin-like growth factor-1 (IGF-1).Frontiers in neuroendocrinology · 2014Review
- Agouti-related peptide plays a critical role in leptin's effects on female puberty and reproduction.American journal of physiology. Endocrinology and metabolism · 2013Article
- Neurokinin B causes acute GnRH secretion and repression of GnRH transcription in GT1-7 GnRH neurons.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Genetic mechanisms mediating kisspeptin regulation of GnRH gene expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Cell-type specific expression of oxytocin and vasopressin genes: an experimental odyssey.Journal of neuroendocrinology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Appropriate tissue-specific gene expression of gonadotropin-releasing hormone (GnRH) is critical for pubertal development and maintenance of reproductive competence. In these studies, a common element in the mouse GnRH (mGnRH) promoter, between -2806 and -2078 bp, is shown to mediate differential regulation of hypothalamic and ovarian mGnRH expression. To further characterize this region, we generated a knock-out mouse (GREKO(-/-)) with a deletion of the mGnRH promoter fragment between -2806 and -2078 bp. GnRH mRNA expression in the brain of GREKO(-/-) was less than the expression in wild-type mice; however, immunohistochemical analysis revealed no difference between the numbers of GnRH neurons among groups. GnRH mRNA expression in the ovary was fivefold higher in GREKO(-/-). The immunohistochemical staining for GnRH in the ovary increased in surface epithelial and granulosa cells and also in the corpora lutea of GREKO(-/-) mice. The reproductive phenotype revealed that the mean day of vaginal opening was delayed, and additionally, there was a significant decrease in the length of proestrus and diestrus-metestrus phases of the estrous cycle, resulting in a shortened estrous cycle in GREKO(-/-) mice. This work supports the hypothesis that the region of the GnRH promoter contained between -2806 and -2078 bp acts as a cell-specific enhancer in the GnRH neuron and as a repressor in the ovary. Deletion of this region in vivo implicates the GnRH promoter in mediating pubertal development and periodic reproductive cycling, and forms the foundation to define the nuclear proteins important for puberty and estrous cycling in mammals.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.