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G protein-coupled estrogen receptor 1 (GPER), also known as G protein-coupled receptor 30 (GPR30), is a protein that in humans is encoded by the GPER gene. GPER binds to and is activated by the female sex hormone estradiol and is responsible for some of the rapid effects that estradiol has on cells.

Role in neurological disorders[edit]
GPER is broadly expressed on the nervous system, and GPER activation promotes beneficial effects in several brain disorders. A study suggests that GPER levels were significantly lower in children with ADHD compared to controls.

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↓ My edits below ↓

I added Intro, 6. Role in neurological disorders

and 7. Role in immune-related diseases (newly)

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G protein-coupled estrogen receptor 1 (GPER), also known as G protein-coupled receptor 30 (GPR30), is a protein that in humans is encoded by the GPER gene. GPER binds to and is activated by the female sex hormone estradiol and is responsible for some of the rapid effects that estradiol has on cells. GPER expresses widely in human body, including reproductive, cardiovascular, endocrine and nervous system. Based on this ubiquitous distribution, GPER is a functional estrogen receptor involved in estrogen related actions on several systems. The expression level of GPER could depend on gender, age and disease types.

Role in neurological disorders[edit]
GPER (mRNA and protein) expression have been detected throughout the central and peripheral nervous system, including in the hippocampus, hypothalamus and midbrain, as well as the spinal cord and dorsal root ganglia. 17β‑Estradiol has many beneficial effects on the brain, including reduction of neuronal loss following stroke, increase in neuronal connectivity and improvement of cognitive performance. GPER has been implicated in 17β‑ estradiol-mediated effects on cholinergic neurons in the basal forebrain. In vivo studies showed that G‑1 treatment replicates the effects of 17β‑estradiol in promoting neuronal survival following global ischemia in the brain. It was demonstrated that GPER selective activation protected hippocampal CA1 pyramidal neurons exposed to ischemia in OVX female rats and mice. Furthermore, G‑1 exhibited antidepressant properties in a mouse model of depression, where it reproduced the effects of 17β‑estradiol, which were inhibited by the GPER-selective antagonist G15.

Role in immune-related diseases
GPER is expressed in peripheral B and T lymphocytes as well as in monocytes, eosinophils, and neutrophils. It has been found to regulate estrogenic effects on specific immune functions, not only in humans but also in various other species. 17β estradiol displays multiple effects in the regulation of immune responses, including the development of T cells, autoimmune disease, and inhibition of inflammation. Studies in Esr1 knockout and Gper knockout mice have shown that GPER, along with ERα, contributes to 17β estradiol-induced thymic atrophy; ERα mediated the early blockage of thymocyte development, whereas GPER mediated thymocyte apoptosis.