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Special Issue "Progesterone Receptor Signaling"
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".
Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 27884
Special Issue Editors
Interests: endometrial regeneration; non-classical progesterone signaling; PGRMC1; pregnancy; uterus
Interests: oviduct; pregnancy; progesterone receptor; single cell RNA-seq; steroid hormone signaling
Special Issue Information
Progesterone receptors (PR) mediate the endocrine actions of the female sex steroid progesterone (P4), which result in cellular and physiological changes to the reproductive system that establish and maintain pregnancy. While many of the actions of P4 are mediated by a classical mechanism involving P4-activated nuclear translocation and transactivation/transrepression of target genes harboring the P4 response element, non-classical P4 signaling mechanisms also occur. While some non-classical mechanisms involve the nuclear PR signaling near the plasma membrane where it modulates various phosphorylation cascades, other non-classical mechanisms involve members of the progesterone receptor membrane component family. Epidemiological and genomic studies in women, as well as conditional mutagenesis studies in rodents not only highlight an essential role of PRs in the development and maintenance of female reproductive organs, fertility, behavior, and immune regulation during pregnancy, they also demonstrate participation of PRs in the development of diseases when disrupted. Indeed, faulty or absent P4 signaling through classical or non-classical mechanism results in a variety of disease states that include endometriosis and women’s reproductive cancers. The objective of this Special Issue is to provide an overview of novel PR signaling mechanisms in diverse reproductive tissues both in the contexts of physiology and pathophysiology
Prof. Dr. James K. Pru
Dr. Wipawee Winuthayanon
Manuscript Submission Information
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- female reproductive tract
- nuclear receptor