A regulatory mechanism of mouse kallikrein 1 gene expression by estrogen.
Estradiol
Estrogen receptor
Kallikrein 1
Uterus
Journal
Molecular and cellular endocrinology
ISSN: 1872-8057
Titre abrégé: Mol Cell Endocrinol
Pays: Ireland
ID NLM: 7500844
Informations de publication
Date de publication:
01 Nov 2023
01 Nov 2023
Historique:
received:
17
06
2023
revised:
08
08
2023
accepted:
10
08
2023
pubmed:
15
8
2023
medline:
15
8
2023
entrez:
14
8
2023
Statut:
ppublish
Résumé
Tissue kallikrein 1 (Klk1) is a serine protease that degrades several proteins including insulin-like growth factor binding protein-3 and extracellular matrix molecules. Klk1 mRNA expression in the mouse uterus was increased by estradiol-17β (E2). The present study aimed to clarify the regulatory mechanism for Klk1 expression by estrogen. The promoter analysis of the 5'-flanking region of Klk1 showed that the minimal promoter of Klk1 existed in the -136/+24 region, and the estrogen-responsive region in the -433/-136 region. Tamoxifen increased Klk1 mRNA expression and the promoter activity, suggesting the involvement of AP-1 sites. Site-directed mutagenesis for the putative AP-1 sites in the -433/-136 region showed that the two putative AP-1 sites were involved in the regulation of Klk1 expression. Binding of estrogen receptor α (ERα) to the -433/-136 region was revealed by Chip assay. These results indicated that ERα bound the two putative AP-1 sites and transactivated Klk1 in the mouse uterus.
Identifiants
pubmed: 37580010
pii: S0303-7207(23)00195-8
doi: 10.1016/j.mce.2023.112044
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
112044Informations de copyright
Copyright © 2023 Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest None.