Bcl6b-KO 基因敲除小鼠

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产品名称

Bcl6b-KO 基因敲除小鼠

产品编号

S-KO-01201

品系全称

C57BL/6JCya-Bcl6bem1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-12029-Bcl6b-B6J-VB

品系状态

使用本品系发表的文献需注明: Bcl6b-KO 基因敲除小鼠 mice (Strain S-KO-01201) 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
B cell CLL/lymphoma 6, member B
基因别称
Bazf
染色体号
Chr 11 (Mouse)
转录本 ID
NCBI: NM_007528 | Ensembl: ENSMUST00000000326
修饰方式
全身性基因敲除
靶向范围
Exon 2~5
敲除长度
~2.0 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:1278332Homozygous null mice display decreased CD4+ and CD8+ cell numbers in the thymus. Homozygous mice for one null allele display decreased secondary responses of memory CD8+ T cells.
BCL6B,也称为B-cell CLL/lymphoma 6 member B,是一种在细胞核内作为序列特异性转录抑制因子发挥作用的基因。BCL6B在多种生物学功能中发挥着关键作用,包括肿瘤抑制、免疫反应、干细胞自我更新以及血管生成等[1]。在肿瘤抑制方面,BCL6B在多种人类癌症中表达下调,其启动子区域的过度甲基化是导致其沉默的原因之一[2]。例如,在胃癌和结直肠癌中,BCL6B的甲基化与肿瘤发生和发展密切相关,其表达的下调与肿瘤的增殖和迁移有关[3,4]。此外,BCL6B的表达缺失也与肝细胞癌的转移和不良预后相关[5]。在免疫反应方面,BCL6B在记忆CD8+ T淋巴细胞的二次应答中起着重要作用,其缺失会导致二次应答的减弱[7]。此外,BCL6B在血管生成中也发挥着重要作用,BCL6B的过表达会抑制内皮细胞的分化和血管样结构的形成[1]。此外,BCL6B还参与调节精原干细胞的增殖,其过表达会促进精原干细胞的增殖[6]。综上所述,BCL6B在肿瘤抑制、免疫反应和血管生成等方面发挥着重要作用,其表达的下调和过度甲基化与多种癌症的发生和发展密切相关。未来,针对BCL6B的研究可能为癌症的治疗和预防提供新的思路和策略。

参考文献:
1. Li, Zhonghao, Wu, Wei, Li, Qiushi, Xiao, Qingzhong, Yan, Yi. 2024. BCL6B-dependent suppression of ETV2 hampers endothelial cell differentiation. In Stem cell research & therapy, 15, 226. doi:10.1186/s13287-024-03832-y. https://pubmed.ncbi.nlm.nih.gov/39075623/
2. Yang, Qingfan, Gao, Jing, Xu, Lixia, Sung, Joseph J Y, Yu, Jun. 2013. Promoter hypermethylation of BCL6B gene is a potential plasma DNA biomarker for gastric cancer. In Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals, 18, 721-5. doi:10.3109/1354750X.2013.853839. https://pubmed.ncbi.nlm.nih.gov/24191714/
3. Gu, Yue, Li, Aifang, Sun, Hui, Zeng, Zongyue, Zhou, Lan. 2018. BCL6B suppresses proliferation and migration of colorectal carcinoma cells through inhibition of the PI3K/AKT signaling pathway. In International journal of molecular medicine, 41, 2660-2668. doi:10.3892/ijmm.2018.3451. https://pubmed.ncbi.nlm.nih.gov/29393377/
4. Wang, Jia, Dong, Ling, Xu, Lixia, Sung, Joseph J Y, Yu, Jun. 2014. B cell CLL/lymphoma 6 member B inhibits hepatocellular carcinoma metastases in vitro and in mice. In Cancer letters, 355, 192-200. doi:10.1016/j.canlet.2014.08.025. https://pubmed.ncbi.nlm.nih.gov/25218345/
5. Cai, Wang-Yu, Lin, Ling-Yun, Wang, Lin, Chen, Mao-Li, Luo, Qi-Cong. 2019. Inhibition of Bcl6b promotes gastric cancer by amplifying inflammation in mice. In Cell communication and signaling : CCS, 17, 72. doi:10.1186/s12964-019-0387-6. https://pubmed.ncbi.nlm.nih.gov/31288844/
6. Yang, Fan, Whelan, Eoin C, Guan, Xuebing, Wu, Xin, Brinster, Ralph L. 2020. FGF9 promotes mouse spermatogonial stem cell proliferation mediated by p38 MAPK signalling. In Cell proliferation, 54, e12933. doi:10.1111/cpr.12933. https://pubmed.ncbi.nlm.nih.gov/33107118/
7. Manders, Peter M, Hunter, Patricia J, Telaranta, Aino I, Ahmed, Rafi, Fearon, Douglas T. 2005. BCL6b mediates the enhanced magnitude of the secondary response of memory CD8+ T lymphocytes. In Proceedings of the National Academy of Sciences of the United States of America, 102, 7418-25. doi:. https://pubmed.ncbi.nlm.nih.gov/15833813/