ArticleMolecular and cellular endocrinology2021
Kiss1 is differentially regulated in male and female mice by the homeodomain transcription factor VAX1.
Article in Molecular and cellular endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Molecular Characterization of Hypothalamic-Pituitary-Ovarian Axis Regulation in the Manchurian Zokor (Genes · 2025Article
- The transcription factor VAX1 in VIP neurons of the suprachiasmatic nucleus impacts circadian rhythm generation, depressive-like behavior, and the reproductive axis in a sex-specific manner in mice.Frontiers in endocrinology · 2023Article
- Deletion of the homeodomain gene Six3 from kisspeptin neurons causes subfertility in female mice.Molecular and cellular endocrinology · 2022Article
- Sexual Dimorphism in Kisspeptin Signaling.Cells · 2022Review
- Circadian Rhythms in the Neuronal Network Timing the Luteinizing Hormone Surge.Endocrinology · 2022Review
- Reproductive Deficits Induced by Prenatal Antimüllerian Hormone Exposure Require Androgen Receptor in Kisspeptin Cells.Endocrinology · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Regulation of Kiss1 transcription is crucial to the development and function of the reproductive axis. The homeodomain transcription factor, ventral anterior homeobox 1 (VAX1), has been implicated as a potential regulator of Kiss1 transcription. However, it is unknown whether VAX1 directly mediates transcription within kisspeptin neurons or works indirectly by acting upstream of kisspeptin neuron populations. This study tested the hypothesis that VAX1 within kisspeptin neurons regulates Kiss1 gene expression. We found that VAX1 acts as a repressor of Kiss1 in vitro and within the male arcuate nucleus in vivo. In female mice, we found that the loss of VAX1 caused a reduction in Kiss1 expression and Kiss1-containing neurons in the anteroventral periventricular nucleus at the time of the preovulatory luteinizing hormone surge, but was compensated by an increase in Kiss1-cFos colocalization. Despite changes in Kiss1 transcription, gonadotropin levels were unaffected and there were no impairments to fertility.
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