ArticleMolecular endocrinology (Baltimore, Md.)2005
The protein kinase C pathway acts through multiple transcription factors to repress gonadotropin-releasing hormone gene expression in hypothalamic GT1-7 neuronal cells.
Article in Molecular endocrinology (Baltimore, Md.), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Leukemia Inhibitory Factor Represses GnRH Gene Expression via cFOS during Inflammation in Male Mice.Neuroendocrinology · 2019Article
- 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
- Neurokinin B causes acute GnRH secretion and repression of GnRH transcription in GT1-7 GnRH neurons.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Androgen receptor repression of gonadotropin-releasing hormone gene transcription via enhancer 1.Molecular and cellular endocrinology · 2012Article
- Androgen receptor repression of GnRH gene transcription.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Dynamic chromatin modifications control GnRH gene expression during neuronal differentiation and protein kinase C signal transduction.Molecular endocrinology (Baltimore, Md.) · 2011Article
- POU homeodomain protein Oct-1 functions as a sensor for cyclic AMP.The Journal of biological chemistry · 2009Article
- Egr-1 binds the GnRH promoter to mediate the increase in gene expression by insulin.Molecular and cellular endocrinology · 2007Article
- Hormonal regulation of clonal, immortalized hypothalamic neurons expressing neuropeptides involved in reproduction and feeding.Molecular neurobiology · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The GnRH gene uses two well-defined regions to target expression to a small population of hypothalamic GnRH neurons: a 173-bp proximal promoter and a 300-bp enhancer localized at approximately -1800 to -1500 bp from the start site. Interaction of multiple factors with the GnRH enhancer and promoter is required to confer neuron-specific expression in vivo and in cells in culture. In addition, the expression of the GnRH gene is regulated by numerous neurotransmitters and hormones. Several of these effectors act through membrane receptors to trigger the protein kinase C pathway, and 12-O-tetradecanoyl phorbol-13-acetate (TPA), a modulator of this pathway, has been shown to suppress GnRH gene expression through the promoter. We find that TPA suppresses expression through the GnRH enhancer as well as the promoter. In the enhancer, an Oct-1 binding site, a Pbx/Prep binding site, Msx/Dlx binding sites, and a previously unidentified protein-binding element at -1793, all contribute to TPA suppression. TPA treatment leads to decreased binding of Oct-1 and Pbx1a/Prep to their sites. However, a complex formed by GT1-7 nuclear extracts on the -1793 site is not affected by TPA treatment. It is known that cooperative interaction among multiple factors is necessary for GnRH gene expression; thus, one mechanism by which TPA suppresses GnRH gene expression is to disengage some of these factors from their cis-regulatory elements.
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Registered trials
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