scispace - formally typeset
O

Orla M. Conneely

Researcher at Baylor College of Medicine

Publications -  131
Citations -  15354

Orla M. Conneely is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Receptor & Progesterone receptor. The author has an hindex of 63, co-authored 131 publications receiving 14726 citations. Previous affiliations of Orla M. Conneely include Texas Medical Center.

Papers
More filters
Journal ArticleDOI

Mice lacking progesterone receptor exhibit pleiotropic reproductive abnormalities.

TL;DR: Results provide direct support for progesterone's role as a pleiotropic coordinator of diverse reproductive events that together ensure species survival.
Journal ArticleDOI

Nurr1 is essential for the induction of the dopaminergic phenotype and the survival of ventral mesencephalic late dopaminergic precursor neurons.

TL;DR: It is demonstrated that Nurr1 functions at the later stages of dopamine cell development to drive differentiation of ventral mesencephalic late dopaminergic precursor neurons, and is essential for specifying commitment of mesENCEphalic precursors to the full dopamine phenotype.
Journal ArticleDOI

Subgroup of Reproductive Functions of Progesterone Mediated by Progesterone Receptor-B Isoform

TL;DR: Progesterone receptors PR-A and PR-B are functionally distinct mediators of progesterone action in vivo and should provide suitable targets for generation of tissue-selective progestins.
Journal ArticleDOI

Dopaminergic and ligand-independent activation of steroid hormone receptors.

TL;DR: In vitro, dopamine faithfully mimicked the effect of progesterone by causing a translocation of chicken progestersone receptor (cPR) from cytoplasm to nucleus, and a serine residue in the cPR was identified that is not necessary for progester one-dependent activation of cPR, but is essential for dopamine activation of this receptor.
Journal ArticleDOI

Defective mammary gland morphogenesis in mice lacking the progesterone receptor B isoform

TL;DR: It is shown that selective activation of PR-A in PRBKO–/– mice is sufficient to elicit normal ovarian and uterine responses to P but results in reduced mammary gland morphogenesis, and that selective modulation ofPR-A activity by progestin agonists may have a protective effect against both uterine and mammaries hyperplasias.