Gpr55-KO 基因敲除小鼠

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产品名称

Gpr55-KO 基因敲除小鼠

产品编号

S-KO-06074

品系全称

C57BL/6JCya-Gpr55em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-227326-Gpr55-B6J-VA

品系状态

使用本品系发表的文献需注明: Gpr55-KO 基因敲除小鼠 mice (Strain S-KO-06074) 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
G protein-coupled receptor 55
基因别称
CTFL,Gm218,Lpir1
染色体号
Chr 1 (Mouse)
转录本 ID
NCBI: NM_001033290 | Ensembl: ENSMUST00000086975
修饰方式
全身性基因敲除
靶向范围
Exon 2
敲除长度
~1.6 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:2685064Mice homozygous for a knock-out allele exhibit increased bone volume due to impaired osteoclast function in male mice. Female mice exhibit a milder phenotype.
GPR55,全称G蛋白偶联受体55,是一种广泛分布于脑和周围组织的G蛋白偶联受体。GPR55被认为是一种新的大麻素受体,与经典的CB1和CB2受体在序列上差异较大,因此被认为是大麻素受体家族的一个新成员。除了被各种外源性大麻素激活外,GPR55还可以被内源性大麻素如花生四烯酸乙醇酰胺(PEA)激活。GPR55在能量平衡、葡萄糖代谢、神经系统、血管、肾脏和骨骼等多种生理过程中发挥作用,并可能与癌症发展和炎症性疼痛有关。近年来,随着对GPR55研究的深入,其在胃肠道生理和病理过程中的作用也引起了广泛关注。

GPR55的内源性配体通常认为是溶血磷脂酰肌醇(LPI),LPI可以通过磷脂酶C或磷脂酶D的降解作用生成大麻素受体配体2-AG或2-AG,因此GPR55、GPR35和CB受体之间通过其天然配体转换相互联系。GPR55的激活可以促进胰岛素、GIP和GLP-1的释放,从而促进GPR55激动剂单药治疗和联合治疗作为一种新型治疗2型糖尿病的方法。此外,GPR55激动剂还可以改善葡萄糖耐量和胰岛素释放,并可能与其他药物联合使用以增强治疗效果。因此,GPR55被认为是治疗肥胖和2型糖尿病的一个有潜力的药物靶点[1][2][3][4][5][6][7][8][9][10]。

参考文献:
1. Rankin, Linda, Fowler, Christopher J. 2020. The Basal Pharmacology of Palmitoylethanolamide. In International journal of molecular sciences, 21, . doi:10.3390/ijms21217942. https://pubmed.ncbi.nlm.nih.gov/33114698/
2. McCloskey, A G, Miskelly, M G, Moore, C B T, Flatt, P R, McKillop, A M. 2020. CRISPR/Cas9 gene editing demonstrates metabolic importance of GPR55 in the modulation of GIP release and pancreatic beta cell function. In Peptides, 125, 170251. doi:10.1016/j.peptides.2019.170251. https://pubmed.ncbi.nlm.nih.gov/31923454/
3. Tudurí, Eva, López, Miguel, Diéguez, Carlos, Nadal, Angel, Nogueiras, Ruben. 2017. GPR55 and the regulation of glucose homeostasis. In The international journal of biochemistry & cell biology, 88, 204-207. doi:10.1016/j.biocel.2017.04.010. https://pubmed.ncbi.nlm.nih.gov/28457969/
4. Wnorowski, Artur, Wójcik, Jakub, Maj, Maciej. 2021. Gene Expression Data Mining Reveals the Involvement of GPR55 and Its Endogenous Ligands in Immune Response, Cancer, and Differentiation. In International journal of molecular sciences, 22, . doi:10.3390/ijms222413328. https://pubmed.ncbi.nlm.nih.gov/34948125/
5. Tudurí, Eva, Imbernon, Monica, Hernández-Bautista, Rene Javier, Diéguez, Carlos, Nogueiras, Rubén. 2017. GPR55: a new promising target for metabolism? In Journal of molecular endocrinology, 58, R191-R202. doi:10.1530/JME-16-0253. https://pubmed.ncbi.nlm.nih.gov/28196832/
6. Zhao, Pingwei, Abood, Mary E. 2012. GPR55 and GPR35 and their relationship to cannabinoid and lysophospholipid receptors. In Life sciences, 92, 453-7. doi:10.1016/j.lfs.2012.06.039. https://pubmed.ncbi.nlm.nih.gov/22820167/
7. Marichal-Cancino, Bruno A, Fajardo-Valdez, Alfonso, Ruiz-Contreras, Alejandra E, Mendez-Díaz, Monica, Prospero-García, Oscar. . Advances in the Physiology of GPR55 in the Central Nervous System. In Current neuropharmacology, 15, 771-778. doi:10.2174/1570159X14666160729155441. https://pubmed.ncbi.nlm.nih.gov/27488130/
8. Hryhorowicz, Szymon, Walczak, Michal, Zakerska-Banaszak, Oliwia, Słomski, Ryszard, Skrzypczak-Zielińska, Marzena. . Pharmacogenetics of Cannabinoids. In European journal of drug metabolism and pharmacokinetics, 43, 1-12. doi:10.1007/s13318-017-0416-z. https://pubmed.ncbi.nlm.nih.gov/28534260/
9. García-Gutiérrez, María S, Navarrete, Francisco, Navarro, Gemma, Giner, Salvador, Manzanares, Jorge. . Alterations in Gene and Protein Expression of Cannabinoid CB2 and GPR55 Receptors in the Dorsolateral Prefrontal Cortex of Suicide Victims. In Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 15, 796-806. doi:10.1007/s13311-018-0610-y. https://pubmed.ncbi.nlm.nih.gov/29435814/
10. Schicho, Rudolf, Storr, Martin. 2012. A potential role for GPR55 in gastrointestinal functions. In Current opinion in pharmacology, 12, 653-8. doi:10.1016/j.coph.2012.09.009. https://pubmed.ncbi.nlm.nih.gov/23063456/