Mylk3-flox 基因敲除小鼠

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产品名称

Mylk3-flox 基因敲除小鼠

产品编号

S-CKO-05714

品系全称

C57BL/6JCya-Mylk3em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-213435-Mylk3-B6J-VA

品系状态

使用本品系发表的文献需注明: Mylk3-flox 基因敲除小鼠 mice (Strain S-CKO-05714) 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
myosin light chain kinase 3
基因别称
D830007F02Rik,MLCK
染色体号
Chr 8 (Mouse)
转录本 ID
NCBI: NM_175441.5 | Ensembl: ENSMUST00000034133
修饰方式
条件性基因敲除
靶向范围
Exon 2~3
敲除长度
~2159 bp
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:2443063Mice homozygous for a knock-out allele exhibit cardiac hypertrophy, reduced cardiac function and increased response of heart to induced stress.
MYLK3,也称为肌球蛋白轻链激酶3,是一种编码心脏肌球蛋白轻链激酶(cMLCK)的基因。cMLCK在心脏收缩功能中发挥重要作用,它通过磷酸化心室肌球蛋白调节轻链(MLC2v)来调节心脏的收缩性。MYLK3的突变与家族性扩张型心肌病(DCM)有关,这是一种以心脏扩大和心力衰竭为特征的疾病。在心脏衰竭患者中,MYLK3的表达水平显著降低,这表明MYLK3的失调可能参与心脏收缩功能障碍的发生。此外,MYLK3的甲基化水平与卵巢癌患者的生存率相关,高甲基化的MYLK3与更好的生存率相关,这可能作为预测手术反应的生物标志物。MYLK3的表达还受到GATA转录因子的调控,这表明MYLK3在红细胞功能和血管发育中可能发挥重要作用。综上所述,MYLK3在心脏功能、疾病发生和红细胞功能中发挥重要作用,对其研究的深入将有助于理解相关疾病的发病机制,并为疾病的治疗和预防提供新的思路和策略[1,2,3,4,5,6,7,8]。

参考文献:
1. Hitsumoto, Tatsuro, Tsukamoto, Osamu, Matsuoka, Ken, Haruta, Jun-Ichi, Takashima, Seiji. 2023. Restoration of Cardiac Myosin Light Chain Kinase Ameliorates Systolic Dysfunction by Reducing Superrelaxed Myosin. In Circulation, 147, 1902-1918. doi:10.1161/CIRCULATIONAHA.122.062885. https://pubmed.ncbi.nlm.nih.gov/37128901/
2. Phelps, David L, Borley, Jane V, Flower, Kirsty J, Brown, Robert, Ghaem-Maghami, Sadaf. 2017. Methylation of MYLK3 gene promoter region: a biomarker to stratify surgical care in ovarian cancer in a multicentre study. In British journal of cancer, 116, 1287-1293. doi:10.1038/bjc.2017.83. https://pubmed.ncbi.nlm.nih.gov/28350786/
3. Ghaderi, Shahrooz, Levkau, Bodo. 2023. An erythrocyte-centric view on the MFSD2B sphingosine-1-phosphate transporter. In Pharmacology & therapeutics, 249, 108483. doi:10.1016/j.pharmthera.2023.108483. https://pubmed.ncbi.nlm.nih.gov/37390971/
4. Min, Kyung-Duk, Asakura, Masanori, Liao, Yulin, Mochizuki, Naoki, Kitakaze, Masafumi. 2010. Identification of genes related to heart failure using global gene expression profiling of human failing myocardium. In Biochemical and biophysical research communications, 393, 55-60. doi:10.1016/j.bbrc.2010.01.076. https://pubmed.ncbi.nlm.nih.gov/20100464/
5. Tobita, Takashige, Nomura, Seitaro, Morita, Hiroyuki, Aburatani, Hiroyuki, Komuro, Issei. 2017. Identification of MYLK3 mutations in familial dilated cardiomyopathy. In Scientific reports, 7, 17495. doi:10.1038/s41598-017-17769-1. https://pubmed.ncbi.nlm.nih.gov/29235529/
6. Tougas, Carson L, Grindrod, Tabor, Cai, Lawrence X, Alkassis, Fariz F, Kasahara, Hideko. 2019. Heterozygous Mylk3 Knockout Mice Partially Recapitulate Human DCM With Heterozygous MYLK3 Mutations. In Frontiers in physiology, 10, 696. doi:10.3389/fphys.2019.00696. https://pubmed.ncbi.nlm.nih.gov/31244672/
7. Williams, Jack L, Paudyal, Anju, Awad, Sherine, Cox, Roger D, Metherell, Lou A. 2020. Mylk3 null C57BL/6N mice develop cardiomyopathy, whereas Nnt null C57BL/6J mice do not. In Life science alliance, 3, . doi:10.26508/lsa.201900593. https://pubmed.ncbi.nlm.nih.gov/32213617/
8. Hajebi Khaniki, Saeedeh, Shokoohi, Farhad, Esmaily, Habibollah, Kerachian, Mohammad Amin. 2023. Analyzing aberrant DNA methylation in colorectal cancer uncovered intangible heterogeneity of gene effects in the survival time of patients. In Scientific reports, 13, 22104. doi:10.1038/s41598-023-47377-1. https://pubmed.ncbi.nlm.nih.gov/38092774/