Ccl1-KO 基因敲除小鼠

下单100%中奖,最高可得千元京东卡
复苏/繁育服务
产品名称

Ccl1-KO 基因敲除小鼠

产品编号

S-KO-04221

品系全称

C57BL/6JCya-Ccl1em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-20290-Ccl1-B6J-VA

品系状态

使用本品系发表的文献需注明: Ccl1-KO 基因敲除小鼠 mice (Strain S-KO-04221) 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
C-C motif chemokine ligand 1
基因别称
I-309,P500,Scya1,Tca-3,Tca3
染色体号
Chr 11 (Mouse)
转录本 ID
NCBI: NM_011329 | Ensembl: ENSMUST00000108189
修饰方式
全身性基因敲除
靶向范围
Exon 1~3
敲除长度
~4.4 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:98258Mice homozygous for a targeted null allele are refractory to the anti-inflammatory response of the statin drug lovastatin and fail to exhibit an increase in regulatory T cell recruitment to sites of inflammation in a model of delayed-type hypersensitivity.
CCL1,也称为I-309,是一种属于C-C趋化因子家族的蛋白质。CCL1在免疫系统中起着关键作用,它通过与其特定的受体CCR8相互作用,参与调节免疫细胞的迁移和功能。CCL1在多种生物学过程中发挥作用,包括免疫监视、炎症反应和肿瘤发生。

CCL1在脑部缺血性中风后,能够促进神经调节性T细胞(Treg)在脑部的积累,进而抑制神经毒性星形胶质细胞增生,增强神经功能恢复[1]。CCL1还在肿瘤细胞外泌体中表达,促进肿瘤细胞在脑部转移灶的定植[2]。此外,CCL1在背根神经节中的表达与神经性疼痛的发生有关,且在女性患者中表达水平更高[3]。CCL1在CD4+ T细胞中的表达受TIM-3的调控,TIM-3过表达的细胞中CCL1的表达水平显著升高[4]。CCL1在自然杀伤细胞中表达,并能通过分泌一系列趋化因子来招募T细胞,增强对膀胱癌细胞的杀伤作用[5]。CCL1在乳腺癌中表达升高,并与肿瘤浸润的免疫抑制性Treg细胞数量相关,提示其可能作为乳腺癌的预后标志物和治疗靶点[6]。CCL1与CCR8相互作用,其结构基础和抗体抑制机制已被研究[7]。此外,在革兰氏阴性细菌中,CCL1的过表达可以绕过CycH对c型细胞色素生物合成的需要[8]。

综上所述,CCL1是一种重要的免疫调节因子,参与调节免疫细胞的迁移和功能,在多种生物学过程中发挥作用。CCL1在脑部缺血性中风、肿瘤转移、神经性疼痛、自身免疫性疾病和细菌生物合成中发挥重要作用。CCL1的研究有助于深入理解免疫系统的调控机制,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Ito, Minako, Komai, Kyoko, Mise-Omata, Setsuko, Shichita, Takashi, Yoshimura, Akihiko. 2019. Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery. In Nature, 565, 246-250. doi:10.1038/s41586-018-0824-5. https://pubmed.ncbi.nlm.nih.gov/30602786/
2. Rodrigues, Gonçalo, Hoshino, Ayuko, Kenific, Candia M, Pisapia, David, Lyden, David. 2019. Tumour exosomal CEMIP protein promotes cancer cell colonization in brain metastasis. In Nature cell biology, 21, 1403-1412. doi:10.1038/s41556-019-0404-4. https://pubmed.ncbi.nlm.nih.gov/31685984/
3. Ray, Pradipta R, Shiers, Stephanie, Caruso, James P, Dougherty, Patrick M, Price, Theodore J. . RNA profiling of human dorsal root ganglia reveals sex differences in mechanisms promoting neuropathic pain. In Brain : a journal of neurology, 146, 749-766. doi:10.1093/brain/awac266. https://pubmed.ncbi.nlm.nih.gov/35867896/
4. Jun, Ka Jung, Lee, Mi Jin, Shin, Dong Chul, Kim, Kyongmin, Park, Sun. 2011. Identification of CCL1 as a Gene Differentially Expressed in CD4 T Cells Expressing TIM-3. In Immune network, 11, 203-9. doi:10.4110/in.2011.11.4.203. https://pubmed.ncbi.nlm.nih.gov/22039368/
5. Wang, Fangming, Zhang, Gang, Xu, Tianli, Li, Jianxing, Xing, Nianzeng. 2024. High and selective cytotoxicity of ex vivo expanded allogeneic human natural killer cells from peripheral blood against bladder cancer: implications for natural killer cell instillation after transurethral resection of bladder tumor. In Journal of experimental & clinical cancer research : CR, 43, 24. doi:10.1186/s13046-024-02955-7. https://pubmed.ncbi.nlm.nih.gov/38245792/
6. Kuehnemuth, Benjamin, Piseddu, Ignazio, Wiedemann, Gabriela M, Jeschke, Udo, Anz, David. 2018. CCL1 is a major regulatory T cell attracting factor in human breast cancer. In BMC cancer, 18, 1278. doi:10.1186/s12885-018-5117-8. https://pubmed.ncbi.nlm.nih.gov/30572845/
7. Sun, Dawei, Sun, Yonglian, Janezic, Eric, Koerber, James T, Masureel, Matthieu. 2023. Structural basis of antibody inhibition and chemokine activation of the human CC chemokine receptor 8. In Nature communications, 14, 7940. doi:10.1038/s41467-023-43601-8. https://pubmed.ncbi.nlm.nih.gov/38040762/
8. Deshmukh, Meenal, May, Matthew, Zhang, Yan, Kranz, Robert G, Daldal, Fevzi. . Overexpression of ccl1-2 can bypass the need for the putative apocytochrome chaperone CycH during the biogenesis of c-type cytochromes. In Molecular microbiology, 46, 1069-80. doi:. https://pubmed.ncbi.nlm.nih.gov/12421312/