What question did this study set out to answer?

To determine whether estrogen directly regulates human corticotropin-releasing hormone gene transcription via estrogen-responsive elements located in its promoter region.

October 1, 1993Journal of Clinical InvestigationOpen Access

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

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To determine whether estrogen directly regulates human corticotropin-releasing hormone gene transcription via estrogen-responsive elements located in its promoter region.
Assayed estrogen-mediated transcriptional activation of 0.9-kb and 2.4-kb 5' flanking human corticotropin-releasing hormone gene segments containing half-palindromic estrogen-responsive elements via chloramphenicol acetyltransferase analysis in transfected CV-1 cells.
Assessed physical interactions between the human estrogen receptor DNA-binding domain and promoter estrogen-responsive elements using in vitro gel retardation and immunoprecipitation.
Estrogen induced transcriptional activation of the 0.9-kb and 2.4-kb promoter segments at levels approximately 10% and 20% of the Xenopus vitellogenin A2 enhancer, respectively.
Gel retardation and immunoprecipitation confirmed specific in vitro binding between the half-palindromic estrogen-responsive elements of the human corticotropin-releasing hormone gene and the human estrogen receptor DNA-binding domain.

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Implication

In vitro molecular study reveals direct estrogenic stimulation of the human corticotropin-releasing hormone gene, indicating a mechanism for sex differences in stress and immune responses.

Cite This Study

Vamvakopoulos et al. (1993) studied this question.

synapsesocial.com/papers/6a10d0e8497e609eda645cc3 https://doi.org/10.1172/jci116782

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Implication

In vitro molecular study reveals direct estrogenic stimulation of the human corticotropin-releasing hormone gene, indicating a mechanism for sex differences in stress and immune responses.

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Key Points

Discussion

Implication

Cite This Study

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Key Points

Discussion

Implication

Cite This Study

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