Hpgds-flox 基因敲除小鼠

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产品名称

Hpgds-flox 基因敲除小鼠

产品编号

S-CKO-17645

品系全称

C57BL/6NCya-Hpgdsem1flox/Cya

品系背景

C57BL/6NCya

品系编号

CKOCMP-54486-Hpgds-B6N-VB

品系状态

使用本品系发表的文献需注明: Hpgds-flox 基因敲除小鼠 mice (Strain S-CKO-17645) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
cKO小鼠库模型

基本信息

基因研究概述

质控标准

基因
基因全称
hematopoietic prostaglandin D synthase
基因别称
H-PGDS,Ptgds2
染色体号
Chr 6 (Mouse)
转录本 ID
NCBI: NM_019455 | Ensembl: ENSMUST00000031982
修饰方式
条件性基因敲除
靶向范围
Exon 2
敲除长度
~1.4 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:1859384Mice homozygous for a knock-out allele display increased IL-2 synthesis and heightened proliferation of ex vivo lymph node cultures in response to BSA or concanavalin A challenge, and fail to resolve a Th1-driven delayed type hypersensitivity reaction.
Hpgds,也称为Hematopoietic prostaglandin D synthase,是血红素加氧酶家族的成员之一,负责催化花生四烯酸转化为前列腺素D2(PGD2)。PGD2是一种重要的炎症介质,参与调节多种生物学过程,包括炎症反应、免疫反应、血管生成和细胞增殖等。Hpgds在多种细胞类型中表达,包括巨噬细胞、肥大细胞和上皮细胞等。

Hpgds在多种疾病中发挥重要作用。例如,Hpgds在动脉粥样硬化中通过NF-κB/IL-6信号通路介导巨噬细胞的炎症反应,促进动脉粥样硬化斑块的形成[1]。在糖尿病心肌病中,Hpgds通过下调lncRNA TINCR抑制焦亡和糖尿病心肌病的发生[2]。在结直肠癌中,Hpgds通过m6A修饰抑制SOX4 mRNA的表达,从而抑制肿瘤的转移[3]。此外,Hpgds的基因多态性与中国儿童Wilms瘤的易感性降低相关[4]。

Hpgds不仅在RNA修饰中发挥作用,还具有独立的染色质调控功能。Hpgds可以与H3K27me3结合,招募KDM6B诱导H3K27me3的去甲基化,从而影响基因表达和干细胞的多能性维持[5]。此外,Hpgds还可以通过下调lncRNA XIST的表达抑制结直肠癌的增殖和转移[6]。

Hpgds在多种疾病中发挥重要作用,包括动脉粥样硬化、糖尿病心肌病、结直肠癌和Wilms瘤。此外,Hpgds还具有独立的染色质调控功能,影响基因表达和干细胞的多能性维持。Hpgds的研究有助于深入理解RNA表观遗传修饰的生物学功能和疾病发生机制,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Huang, Chun, Ge, Fei, Ren, Wenwen, Yan, Ping, Liang, Chunnian. 2020. Copy number variation of the HPGDS gene in the Ashidan yak and its associations with growth traits. In Gene, 772, 145382. doi:10.1016/j.gene.2020.145382. https://pubmed.ncbi.nlm.nih.gov/33373661/
2. Ouyang, Long, Qiu, Daojing, Fu, Xin, Yan, Li, Xiao, Ran. 2022. Overexpressing HPGDS in adipose-derived mesenchymal stem cells reduces inflammatory state and improves wound healing in type 2 diabetic mice. In Stem cell research & therapy, 13, 395. doi:10.1186/s13287-022-03082-w. https://pubmed.ncbi.nlm.nih.gov/35922870/
3. Xie, Zhenyu, Niu, Liaoran, Zheng, Gaozan, Zhang, Jian, Zheng, Jianyong. 2023. Single-cell analysis unveils activation of mast cells in colorectal cancer microenvironment. In Cell & bioscience, 13, 217. doi:10.1186/s13578-023-01144-x. https://pubmed.ncbi.nlm.nih.gov/38031173/
4. Shao, Fengling, Mao, Huajie, Luo, Tengling, Xu, Lei, Xie, Yajun. 2022. HPGDS is a novel prognostic marker associated with lipid metabolism and aggressiveness in lung adenocarcinoma. In Frontiers in oncology, 12, 894485. doi:10.3389/fonc.2022.894485. https://pubmed.ncbi.nlm.nih.gov/36324576/
5. Liu, Yong, Liang, Youcheng, Su, Yongjian, Zheng, Mingbin, Huang, Zunnan. 2023. Exploring the potential mechanisms of Yi-Yi-Fu-Zi-Bai-Jiang-San therapy on the immune-inflamed phenotype of colorectal cancer via combined network pharmacology and bioinformatics analyses. In Computers in biology and medicine, 166, 107432. doi:10.1016/j.compbiomed.2023.107432. https://pubmed.ncbi.nlm.nih.gov/37729701/
6. Yazdanpanah, Nahid, Jumentier, Basile, Yazdanpanah, Mojgan, Perry, John R B, Manousaki, Despoina. 2024. Mendelian randomization identifies circulating proteins as biomarkers for age at menarche and age at natural menopause. In Communications biology, 7, 47. doi:10.1038/s42003-023-05737-7. https://pubmed.ncbi.nlm.nih.gov/38184718/