NK3R (Neurokinin 3 Receptor) Antibody
- Known as:
- NK3R (Neurokinin 3 Receptor) Antibody
- Catalog number:
- 20061
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Immunostar
- Gene target:
- NK3R (Neurokinin 3 Receptor) Antibody
Related genes to: NK3R (Neurokinin 3 Receptor) Antibody
- Gene:
- TACR3 NIH gene
- Name:
- tachykinin receptor 3
- Previous symbol:
- -
- Synonyms:
- NK3R, NKR, TAC3R, NK3
- Chromosome:
- 4q24
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-28
- Date modifiied:
- 2018-02-28
Related products to: NK3R (Neurokinin 3 Receptor) Antibody
Related articles to: NK3R (Neurokinin 3 Receptor) Antibody
- Hypogonadotropic hypogonadism (HH) is due to impaired gonadotropin releasing hormone (GnRH) action resulting in absent puberty and infertility. At least 44 genes have been identified to possess genetic variants in 40-50% of nHH/KS, and 2-20% have presumed digenic disease, but not all variants have been characterized in vitro. - Source: PubMed
Publication date: 2024/04/07
Poch AlexandraDougherty Michael PRoman Robert AChorich LynnHawkins ZoeKim Soo-HyunKim Hyung-GooLayman Lawrence C - Tachykinin receptor 3 (TACR3) is a member of the tachykinin receptor family and falls within the rhodopsin subfamily. As a G protein-coupled receptor, it responds to neurokinin B (NKB), its high-affinity ligand. Dysfunctional TACR3 has been associated with pubertal failure and anxiety, yet the mechanisms underlying this remain unclear. Hence, we have investigated the relationship between TACR3 expression, anxiety, sex hormones, and synaptic plasticity in a rat model, which indicated that severe anxiety is linked to dampened TACR3 expression in the ventral hippocampus. TACR3 expression in female rats fluctuates during the estrous cycle, reflecting sensitivity to sex hormones. Indeed, in males, sexual development is associated with a substantial increase in hippocampal TACR3 expression, coinciding with elevated serum testosterone and a significant reduction in anxiety. TACR3 is predominantly expressed in the cell membrane, including the presynaptic compartment, and its modulation significantly influences synaptic activity. Inhibition of TACR3 activity provokes hyperactivation of CaMKII and enhanced AMPA receptor phosphorylation, associated with an increase in spine density. Using a multielectrode array, stronger cross-correlation of firing was evident among neurons following TACR3 inhibition, indicating enhanced connectivity. Deficient TACR3 activity in rats led to lower serum testosterone levels, as well as increased spine density and impaired long-term potentiation (LTP) in the dentate gyrus. Remarkably, aberrant expression of functional TACR3 in spines results in spine shrinkage and pruning, while expression of defective TACR3 increases spine density, size, and the magnitude of cross-correlation. The firing pattern in response to LTP induction was inadequate in neurons expressing defective TACR3, which could be rectified by treatment with testosterone. In conclusion, our study provides valuable insights into the intricate interplay between TACR3, sex hormones, anxiety, and synaptic plasticity. These findings highlight potential targets for therapeutic interventions to alleviate anxiety in individuals with TACR3 dysfunction and the implications of TACR3 in anxiety-related neural changes provide an avenue for future research in the field. - Source: PubMed
Publication date: 2023/12/22
Wojtas Magdalena NataliaDiaz-González MartaStavtseva NadezhdaShoam YuvalVerma PoonamBuberman AssafIzhak InbarGeva AriaBasch RoiOuro AlbertoPerez-Benitez LuciaLevy UriBorcel ErikaNuñez ÁngelVenero CesarRotem-Dai NoaVeksler-Lublinsky IsanaKnafo Shira - Neurokinin B (NKB), a peptide encoded by the tachykinin 3 (TAC3), is critical for reproduction in all studied species. However, its potential roles in birds are less clear. Using the female chicken (c-) as a model, we showed that cTAC3 is composed of five exons with a full-length cDNA of 787 bp, which was predicted to generate the mature NKB peptide containing 10 amino acids. Using cell-based luciferase reporter assays, we demonstrated that cNKB could effectively and specifically activate tachykinin receptor 3 (TACR3) in HEK293 cells, suggesting its physiological function is likely achieved via activating cTACR3 signaling. Notably, cTAC3 and cTACR3 were predominantly and abundantly expressed in the hypothalamus of hens and meanwhile the mRNA expression of cTAC3 was continuously increased during development, suggesting that NKB-TACR3 may emerge as important components of the neuroendocrine reproductive axis. In support, intraperitoneal injection of cNKB could significantly promote hypothalamic cGnRH-Ι, and pituitary cFSHβ and cLHβ expression in female chickens. Surprisingly, cTAC3 and cTACR3 were also expressed in the pituitary gland, and cNKB treatment significantly increased cLHβ and cFSHβ expression in cultured primary pituitary cells, suggesting cNKB can also act directly at the pituitary level to stimulate gonadotropin synthesis. Collectively, our results reveal that cNKB functionally regulate GnRH/gonadotropin synthesis in female chickens. - Source: PubMed
Publication date: 2023/12/17
Meng FengyanLi JinxuanHan XingfaLi LingyangLi TianyangDu XiaogangCao XiaohanLiang QiuxiaHuang AnqiKong FanliZeng XianyinBu Guixian - The transcriptional profiles of Kiss1 neurons from the arcuate and the rostral periventricular region of the third ventricle of the hypothalamus have been directly compared in diestrous female mice. Differentially expressed genes provide molecular signatures for these two populations of Kiss1 neurons and insights into their physiology. - Source: PubMed
Publication date: 2023/12/15
Manchishi StephenPrater MalwinaColledge William Henry - Vasomotor symptoms (VMS) can often significantly impact women's quality of life at menopause. In vivo studies have shown that increased neurokinin B (NKB) / neurokinin 3 receptor (NK3R) signalling contributes to VMS, with previous genetic studies implicating the TACR3 gene locus that encodes NK3R. Large-scale genomic analyses offer the possibility of biological insights but few such studies have collected data on VMS, while proxy phenotypes such as hormone replacement therapy (HRT) use are likely to be affected by changes in clinical practice. We investigated the genetic basis of VMS by analysing routinely-collected health records. - Source: PubMed
Publication date: 2023/10/02
Ruth Katherine SBeaumont Robin NLocke Jonathan MTyrrell JessicaCrandall Carolyn JHawkes GarethFrayling Timothy MPrague Julia KPatel Kashyap AWood Andrew RWeedon Michael NMurray Anna