Mechanism of gonadotropin-releasing hormone (GnRH)-I and -II-induced cell growth inhibition in ovarian cancer cells: role of the GnRH-I receptor and protein kinase C pathway

Glucocorticoids differentially regulate expression of duodenal and renal calbindin-D9k through glucocorticoid receptor-mediated pathway in mouse model

Impact of environmental endocrine disruption on the reproductive system for human health

Biology and physiology of Calbindin-D9k in female reproductive tissues: Involvement of steroids and endocrine disruptors

A calcium binding protein, Calbindin-D9k, is mainly regulated by estrogen in the pituitary gland of rats during estrous cycle

Maternal exposure to bisphenol A during late pregnancy resulted in an increase of Calbindin-D-9k mRNA and protein in maternal and postnatal rat uteri

Gonadotropins upregulate the epidermal growth factor receptor through activation of mitogen-activated protein kinases and phosphatidyl-inositol-3-kinase in human ovarian surface epithelial cells

Estrogen receptor alpha pathway is involved in the regulation of Calbindin-D-9k in the uterus of immature rats

Conflict of estrogenic activity by various phthalates between in vitro and in vivo models related to the expression of Calbindin-D-9k

Extracellular signal-regulated protein kinase, but not c-JunN-terminal kinase, is activated by type II gonadotropin-releasing hormone involved in the inhibition of ovarian cancer cell proliferation