Itgb4-KO 基因敲除小鼠

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产品名称

Itgb4-KO 基因敲除小鼠

产品编号

S-KO-18108

品系全称

C57BL/6JCya-Itgb4em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-192897-Itgb4-B6J-VA

品系状态

使用本品系发表的文献需注明: Itgb4-KO 基因敲除小鼠 mice (Strain S-KO-18108) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
KO小鼠库模型
PI3K-Akt信号通路

基本信息

基因研究概述

质控标准

基因
基因全称
integrin beta 4
基因别称
C230078O20,CD104
染色体号
Chr 11 (Mouse)
转录本 ID
NCBI: NM_001005608 | Ensembl: ENSMUST00000169928
修饰方式
全身性基因敲除
靶向范围
Exon 3~7
敲除长度
~2.5 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:96613Homozygotes for targeted null mutations die shortly after birth with extensive detachment of the epidermis and other squamus epithelia. Stratified tissues lack hemidesmosomes and simple epithelia are also defective in adherence.
ITGB4,也称为整合素β4,是一种重要的细胞黏附分子,属于整合素家族。整合素是一类跨膜蛋白,在细胞与细胞之间以及细胞与细胞外基质之间的相互作用中发挥着重要作用。ITGB4与α6亚基形成异二聚体,即α6β4整合素,这种整合素在多种细胞过程中发挥重要作用,包括细胞迁移、侵袭、增殖、凋亡以及细胞与细胞外基质的相互作用。

研究表明,ITGB4的表达和功能与多种癌症的发生和发展密切相关。例如,ITGB4在前列腺癌、乳腺癌、肺癌、食管癌和结直肠癌等癌症中表达异常,且与癌症的侵袭、转移和不良预后相关。在前列腺癌中,研究发现ITGB4基因启动子区域的甲基化水平在不同阶段的前列腺肿瘤进展中存在差异,且与ITGB4的表达水平相关[1]。此外,ITGB4在肿瘤相关成纤维细胞中的过表达可以诱导线粒体自噬和乳酸产生,从而促进肿瘤的进展[2]。在肺癌中,ITGB4的表达与脑转移的发生相关,且ITGB4的表达可以预测接受抗PD-1治疗的患者预后[3][4]。在食管癌中,NEDD4L通过介导ITGB4的泛素化降解来抑制食管癌的进展[5]。在结直肠癌中,MDFI通过结合ITGB4和LAMB3来激活AKT信号通路,从而促进结直肠癌细胞增殖和对化疗的耐受性[6]。

此外,ITGB4在头颈癌中发挥重要作用,其表达与EGFR/MAPK活性相关,且ITGB4的表达可以预测对Cetuximab治疗的反应[7]。在遗传性大疱性表皮松解症(EB)中,ITGB4基因突变与EB的发生相关[8]。

综上所述,ITGB4在多种癌症的发生和发展中发挥着重要作用,其表达和功能与癌症的侵袭、转移和不良预后相关。ITGB4的研究有助于深入理解癌症的发生和发展机制,为癌症的治疗和预防提供新的思路和策略。

参考文献:
1. Wilkinson, Emma J, Woodworth, Alexandra M, Parker, Madeline, Dickinson, Joanne L, Holloway, Adele F. 2020. Epigenetic regulation of the ITGB4 gene in prostate cancer. In Experimental cell research, 392, 112055. doi:10.1016/j.yexcr.2020.112055. https://pubmed.ncbi.nlm.nih.gov/32376286/
2. Sung, Jin Sol, Kang, Chan Woo, Kang, Suki, Kim, Baek Gil, Cho, Nam Hoon. 2019. ITGB4-mediated metabolic reprogramming of cancer-associated fibroblasts. In Oncogene, 39, 664-676. doi:10.1038/s41388-019-1014-0. https://pubmed.ncbi.nlm.nih.gov/31534187/
3. Zhang, Jingjing, Li, Lingjie, Luo, Weiwei, Ma, Shenglin, Zhao, Yanyan. 2024. ITGB4 is a prognostic biomarker and correlated with lung adenocarcinoma brain metastasis. In Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 26, 2979-2992. doi:10.1007/s12094-024-03527-z. https://pubmed.ncbi.nlm.nih.gov/38776034/
4. Lu, Xuan, Ma, Sai, Li, Ying, Pan, Yunzhi, Kang, Ningning. 2023. Identification of ITGB4 as a novel tumor promoting gene in lung adenocarcinoma (LUAD). In Oncology reports, 51, . doi:10.3892/or.2023.8689. https://pubmed.ncbi.nlm.nih.gov/38131229/
5. Shi, Yijun, Fang, Na, Wu, Yutong, Chu, Minjie, Cui, Jiahua. 2024. NEDD4L mediates ITGB4 ubiquitination and degradation to suppress esophageal carcinoma progression. In Cell communication and signaling : CCS, 22, 302. doi:10.1186/s12964-024-01685-9. https://pubmed.ncbi.nlm.nih.gov/38831335/
6. Ma, Ding, Liu, Shuwen, Liu, Kua, Jiang, Chunping, Wu, Junhua. 2024. MDFI promotes the proliferation and tolerance to chemotherapy of colorectal cancer cells by binding ITGB4/LAMB3 to activate the AKT signaling pathway. In Cancer biology & therapy, 25, 2314324. doi:10.1080/15384047.2024.2314324. https://pubmed.ncbi.nlm.nih.gov/38375821/
7. Schinke, Henrik, Shi, Enxian, Lin, Zhongyang, Pan, Min, Gires, Olivier. 2022. A transcriptomic map of EGFR-induced epithelial-to-mesenchymal transition identifies prognostic and therapeutic targets for head and neck cancer. In Molecular cancer, 21, 178. doi:10.1186/s12943-022-01646-1. https://pubmed.ncbi.nlm.nih.gov/36076232/
8. Chen, Fuying, Wei, Ruoqu, Deng, Dan, Yao, Zhirong, Li, Ming. 2022. Genotype and phenotype correlations in 441 patients with epidermolysis bullosa from China. In Journal of the European Academy of Dermatology and Venereology : JEADV, 37, 411-419. doi:10.1111/jdv.18692. https://pubmed.ncbi.nlm.nih.gov/36287101/