Bcat2-flox 基因敲除小鼠

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产品名称

Bcat2-flox 基因敲除小鼠

产品编号

S-CKO-01394

品系全称

C57BL/6NCya-Bcat2em1flox/Cya

品系背景

C57BL/6NCya

品系编号

CKOCMP-12036-Bcat2-B6N-VA

品系状态

使用本品系发表的文献需注明: Bcat2-flox 基因敲除小鼠 mice (Strain S-CKO-01394) 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
branched chain aminotransferase 2, mitochondrial
基因别称
Bcat(m),Bcat-2,Eca40
染色体号
Chr 7 (Mouse)
转录本 ID
NCBI: NM_009737 | Ensembl: ENSMUST00000033098
修饰方式
条件性基因敲除
靶向范围
Exon 4~6
敲除长度
~1.2 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:1276534The metabolism of branched chain amino acid is impaired in homozygous null mice, resulting in a phenotype similar to human maple syrup urine disease. Mutants exhibit a failure to thrive and die prematurely, though the severity of the symptoms can be ameliorated with a restricted diet.
BCAT2(Branched-chain amino acid transaminase 2),也称为分支链氨基酸转氨酶2,是一种在分支链氨基酸(BCAA)代谢中发挥关键作用的酶。BCAA包括亮氨酸、异亮氨酸和缬氨酸,是人体必需的氨基酸,参与蛋白质合成、能量代谢和细胞信号传导等重要生理过程。BCAT2通过催化BCAA转化为相应的α-酮酸,参与BCAA的降解和利用。BCAT2的表达和活性受到多种因素的调控,包括营养状态、激素水平和基因变异等。

BCAT2在多种肿瘤的发生和发展中发挥重要作用。例如,研究表明,BCAT2在胰腺导管腺癌(PDAC)中表达上调,并通过促进BCAA的摄取和降解,维持线粒体呼吸和肿瘤细胞的生长[1]。此外,BCAT2还与急性髓系白血病(AML)的发生和发展密切相关。METTL16是一种m6A甲基转移酶,可以促进BCAT1和BCAT2的表达,并通过重新编程BCAA代谢促进AML的发生和发展[2]。在结直肠癌(CRC)中,BCAT2的表达下调,导致BCAA的积累和mTORC1信号通路的持续激活,从而促进肿瘤的发生和发展[3]。此外,BCAT2还与肥胖和银屑病的发生和发展相关。研究表明,高脂饮食诱导的肥胖小鼠表现出更严重的银屑病样病变,并且BCAA代谢通路被抑制,BCAT2的表达下调[4]。此外,BCAT2还与前列腺癌(PCa)的发生和发展相关。研究表明,BCAT2在PCa中表达上调,并与不良预后相关[6]。此外,BCAT2还与多种代谢性疾病的发生和发展相关。研究表明,BCAT2基因多态性与肥胖、胰岛素抵抗和高血压等代谢性疾病的发生和发展相关[5][7]。例如,BCAT2基因的rs11548193多态性与肥胖和胰岛素抵抗的发生和发展相关,并且可以影响饮食干预后BCAA的浓度[7]。

BCAT2在多种生物学过程中发挥重要作用,包括肿瘤的发生和发展、代谢性疾病的发生和发展等。BCAT2的表达和活性受到多种因素的调控,包括营养状态、激素水平和基因变异等。BCAT2的研究有助于深入理解BCAA代谢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. Li, Jin-Tao, Yin, Miao, Wang, Di, Su, Dan, Lei, Qun-Ying. 2020. BCAT2-mediated BCAA catabolism is critical for development of pancreatic ductal adenocarcinoma. In Nature cell biology, 22, 167-174. doi:10.1038/s41556-019-0455-6. https://pubmed.ncbi.nlm.nih.gov/32029896/
2. Han, Li, Dong, Lei, Leung, Keith, Chen, Jianjun, Deng, Xiaolan. . METTL16 drives leukemogenesis and leukemia stem cell self-renewal by reprogramming BCAA metabolism. In Cell stem cell, 30, 52-68.e13. doi:10.1016/j.stem.2022.12.006. https://pubmed.ncbi.nlm.nih.gov/36608679/
3. Kang, Zi-Ran, Jiang, Shanshan, Han, Ji-Xuan, Chen, Huimin, Fang, Jing-Yuan. 2023. Deficiency of BCAT2-mediated branched-chain amino acid catabolism promotes colorectal cancer development. In Biochimica et biophysica acta. Molecular basis of disease, 1870, 166941. doi:10.1016/j.bbadis.2023.166941. https://pubmed.ncbi.nlm.nih.gov/37926361/
4. Wang, Yazhuo, Zhao, Ning, Meng, Yujiao, Li, Ping, Wang, Yan. 2024. Bcat2-Mediated Branched-Chain Amino Acid Catabolism Is Linked to the Aggravated Inflammation in Obese with Psoriasis Mice. In Molecular nutrition & food research, 68, e2300720. doi:10.1002/mnfr.202300720. https://pubmed.ncbi.nlm.nih.gov/38581348/
5. Vargas-Morales, Juan M, Guizar-Heredia, Rocio, Méndez-García, Ana L, Guevara-Cruz, Martha, Noriega, Lilia G. 2021. Association of BCAT2 and BCKDH polymorphisms with clinical, anthropometric and biochemical parameters in young adults. In Nutrition, metabolism, and cardiovascular diseases : NMCD, 31, 3210-3218. doi:10.1016/j.numecd.2021.07.011. https://pubmed.ncbi.nlm.nih.gov/34511290/
6. Dong, Baijun, Xu, Jun-Yu, Huang, Yuqi, Tan, Minjia, Qin, Jun. 2024. Integrative proteogenomic profiling of high-risk prostate cancer samples from Chinese patients indicates metabolic vulnerabilities and diagnostic biomarkers. In Nature cancer, 5, 1427-1447. doi:10.1038/s43018-024-00820-2. https://pubmed.ncbi.nlm.nih.gov/39242942/
7. González-Salazar, Luis E, Granados-Portillo, Omar, Medina-Vera, Isabel, Tovar, Armando R, Guevara-Cruz, Martha. 2021. Effect of the BCAT2 polymorphism (rs11548193) on plasma branched-chain amino acid concentrations after dietary intervention in subjects with obesity and insulin resistance. In The British journal of nutrition, 128, 43-54. doi:10.1017/S0007114521002920. https://pubmed.ncbi.nlm.nih.gov/34340727/