Npffr1-KO 基因敲除小鼠

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产品名称

Npffr1-KO 基因敲除小鼠

产品编号

S-KO-06890

品系全称

C57BL/6JCya-Npffr1em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-237362-Npffr1-B6J-VA

品系状态

使用本品系发表的文献需注明: Npffr1-KO 基因敲除小鼠 mice (Strain S-KO-06890) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量

基本信息

基因研究概述

质控标准

基因
基因全称
neuropeptide FF receptor 1
基因别称
Gm236,Gpr147,NPFF1,NPFF1R,OT7T022
染色体号
Chr 10 (Mouse)
转录本 ID
NCBI: NM_001177511 | Ensembl: ENSMUST00000020287
修饰方式
全身性基因敲除
靶向范围
Exon 3
敲除长度
~0.8 kb
品系说明
该品系是基于策略设计时的数据库信息制作而成,建议您在购买前查询最新的数据库和相关文献,以获取最准确的表型信息。
表型提示
MGI:2685082Mice homozygous for a null mutation display abnormal pituitary function with abnormal levels of follicle stimulating and luteinizing hormone levels and increased litter sizes.
Npffr1,也称为GPR147,是一种重要的七次跨膜G蛋白偶联受体。Npffr1是GnIH(gonadotropin-inhibitory hormone)和NPFF(neuropeptide FF)的受体,这两种神经肽均具有C端LPXRFamide(X=L或Q)结构[1]。Npffr1的激活抑制cAMP的产生,从而发挥其生理功能。

Npffr1在多种生物学过程中发挥作用,包括生殖、疼痛调制、心血管调节和情绪调节等。Npffr1在生殖系统中的功能主要体现在抑制促性腺激素的分泌,从而调节生殖轴的功能[1,6]。此外,Npffr1还参与疼痛调制,与NPFF一起调节痛觉和镇痛作用[3]。在心血管系统中,Npffr1通过调节NPFF的活性,影响心血管功能[4]。在情绪调节方面,Npffr1的激活可以导致抑郁和焦虑行为[7]。

近年来,研究发现Npffr1的基因多态性与多种疾病的发生发展相关。例如,Npffr1的基因多态性与女孩的特发性中枢性性早熟(iCPP)的发生相关[2,6]。此外,Npffr1的基因多态性还与高脂血症的风险相关[5]。这些研究结果表明,Npffr1的基因多态性可能影响个体对疾病的易感性。

综上所述,Npffr1是一种重要的七次跨膜G蛋白偶联受体,参与调节多种生物学过程,包括生殖、疼痛调制、心血管调节和情绪调节等。Npffr1的基因多态性与多种疾病的发生发展相关,为疾病的治疗和预防提供了新的思路和策略。

参考文献:
1. Ubuka, Takayoshi, Tsutsui, Kazuyoshi. 2014. Evolution of gonadotropin-inhibitory hormone receptor and its ligand. In General and comparative endocrinology, 209, 148-61. doi:10.1016/j.ygcen.2014.09.002. https://pubmed.ncbi.nlm.nih.gov/25220854/
2. Toutoudaki, Konstantina, Paltoglou, George, Papadimitriou, Dimitrios T, Tsarna, Ermioni, Christopoulos, Panagiotis. 2023. The Role of SNPs in the Pathogenesis of Idiopathic Central Precocious Puberty in Girls. In Children (Basel, Switzerland), 10, . doi:10.3390/children10030450. https://pubmed.ncbi.nlm.nih.gov/36980008/
3. Ayachi, Safia, Simonin, Frédéric. 2014. Involvement of Mammalian RF-Amide Peptides and Their Receptors in the Modulation of Nociception in Rodents. In Frontiers in endocrinology, 5, 158. doi:10.3389/fendo.2014.00158. https://pubmed.ncbi.nlm.nih.gov/25324831/
4. Zegeye, Tsadkan, Belay, Gurja, Vallejo-Trujillo, Adriana, Han, Jianlin, Hanotte, Olivier. 2023. Genome-wide diversity and admixture of five indigenous cattle populations from the Tigray region of northern Ethiopia. In Frontiers in genetics, 14, 1050365. doi:10.3389/fgene.2023.1050365. https://pubmed.ncbi.nlm.nih.gov/37600659/
5. Curtis, David. 2020. Analysis of exome-sequenced UK Biobank subjects implicates genes affecting risk of hyperlipidaemia. In Molecular genetics and metabolism, 131, 277-283. doi:10.1016/j.ymgme.2020.07.009. https://pubmed.ncbi.nlm.nih.gov/32747172/
6. Lima, C J G, Cardoso, S C, Lemos, E F L, Latronico, A C, Lofrano-Porto, A. . Mutational analysis of the genes encoding RFamide-related peptide-3, the human orthologue of gonadotrophin-inhibitory hormone, and its receptor (GPR147) in patients with gonadotrophin-releasing hormone-dependent pubertal disorders. In Journal of neuroendocrinology, 26, 817-24. doi:10.1111/jne.12207. https://pubmed.ncbi.nlm.nih.gov/25180599/
7. Lin, Ya-Tin, Liu, Tzu-Yu, Yang, Ching-Yao, Huang, Guo-Jen, Chen, Jin-Chung. 2016. Chronic activation of NPFFR2 stimulates the stress-related depressive behaviors through HPA axis modulation. In Psychoneuroendocrinology, 71, 73-85. doi:10.1016/j.psyneuen.2016.05.014. https://pubmed.ncbi.nlm.nih.gov/27243477/