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The inherited basis of hypergonadotropic hypogonadism
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
The clinical phenotypes of PROKR2/PROK2 mutations, encoding prokineticin receptor-2 and prokineticin-2, respectively, range from both classical KS to normosmic hypogonadotropic hypogonadism.59 Nonreproductive phenotypes include fibrous dysplasia, bimanual synkinesia, and epilepsy. Patients with the more severe reproductive dysfunction tend to have biallelic mutations in PROK2/PROKR2 and fewer associated nonreproductive abnormalities. Patients with monoallelic mutations have less severe reproductive dysfunction and more nonreproductive abnormalities. The PROKR2 is a G protein–coupled receptor that binds to the ligand PROK2. Mouse prok2 knockout models have small, abnormally shaped olfactory bulbs with an accumulation of neurons in the rostral migratory stream (RMS) between the sub-ventricular zone and the olfactory bulb.60
Prokineticin 2 relieves hypoxia/reoxygenation-induced injury through activation of Akt/mTOR pathway in H9c2 cardiomyocytes
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2020
Gang Su, Guangli Sun, Hai Liu, Liliang Shu, Weiwei Zhang, Zhenxing Liang
Prokineticin 2 (PK2), also known as Bv8, is a small chemokine-like secreted protein that exerts its biological activities via activation of two cognate G protein-linked receptors, namely prokineticin receptor 1 (PKR1) and 2 (PKR2) [5]. PK2 is well-documented to be highly expressed in activated immune cells and inflamed murine tissues with infiltrating neutrophils, showing proinflammatory activities via PKR1 [6]. Recent literatures report that PK2 is also implicated in regulating diverse essential physiological and/or pathological processes, including circadian rhythms, neuroprotection, angiogenesis and pain perception [7–10]. More importantly, it was reported that the expression of PK2 and its receptors were decreased in the hearts of end-state heart failure patients [11]. PK2 activated the protein kinase B (Akt) pathway to prevent cardiomyocytes from apoptosis against hypoxic insult [11]. Still, little is known about the effects of PK2 on I/R injury in AMI.
Direct and indirect evidences of BDNF and NGF as key modulators in depression: role of antidepressants treatment
Published in International Journal of Neuroscience, 2019
Amal Chandra Mondal, Mahino Fatima
Nerve growth factor level is increased with AD treatment [24] and also, NGF itself acts as AD in rats [28]. Administration of NGF improves depressive behavior in rats by modifying the gene expression of Drd5, Prokr1, Htr3a, Chrna5, Maoa, Chrnb4, Sstr3, and Cckar in amygdala and hippocampus. Simultaneously, NGF reduces the expression of cholinergic gene CHRNA5 following fluoxetine treatment and decreases in prokineticin receptor 1 (PROKR1) by amitriptyline treatment [123]. Nerve growth factor improves mood and cognition and its involvement in anxiety disorder is evident as children with one or more copies of allele NGF rs6330 have lesser susceptibility to develop anxiety [124]. Inconsistency in data related to stress-dependent alterations of serum NGF in humans has been evident as its level has found to be increased [125] or unchanged [126,127] during acute stress. Thus, alterations in NGF could be considered as key factor in the progression of depressive disorders and NGF polymorphism rs6330 and serum NGF levels may be predictor of efficient psychological therapies, provided with consistent control [128,129]. Figure 2 shows involvement of NGF mediated signaling patways in depression and effect of ADs treatment on neurogenesis.