Tspyl5-KO 基因敲除小鼠

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产品名称

Tspyl5-KO 基因敲除小鼠

产品编号

S-KO-07066

品系全称

C57BL/6NCya-Tspyl5em1/Cya

品系背景

C57BL/6NCya

品系编号

KOCMP-239364-Tspyl5-B6N-VA

品系状态

使用本品系发表的文献需注明: Tspyl5-KO 基因敲除小鼠 mice (Strain S-KO-07066) 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
testis-specific protein, Y-encoded-like 5
基因别称
6330530B20,E130308C19Rik
染色体号
Chr 15 (Mouse)
转录本 ID
NCBI: NM_001085421 | Ensembl: ENSMUST00000042021
修饰方式
全身性基因敲除
靶向范围
Exon 1
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:2442458Homozygous null males show reduced fertility with age, with reduced spermatogonia and sperm counts, reduced spermatogonia proliferation, and abnormal seminiferous tubule morphology.
Tspyl5基因编码的蛋白属于核小体组装蛋白家族,其具体功能尚不完全清楚。研究表明,Tspyl5基因的表达和甲基化状态与多种癌症的发生、发展和治疗耐药性相关。例如,在胃癌中,Tspyl5基因的表达水平常被下调,且与DNA甲基化呈负相关[1]。此外,在前列腺癌中,Tspyl5基因的表达也受到DNA甲基化的调控,其低表达与肿瘤的进展和药物敏感性下降相关[2]。在肺癌中,Tspyl5基因的表达水平与细胞对辐射的敏感性相关,其低表达会导致细胞对辐射的抵抗性增加[3]。在乳腺癌中,Tspyl5基因的表达与患者的预后相关,高表达是预后不良的独立指标[4]。在结直肠癌中,Tspyl5基因的表达水平也与患者的预后相关,低表达提示预后不良[5]。

在肺癌中,Tspyl5基因的表达水平与肿瘤干细胞样特征相关,高表达会维持肿瘤干细胞的特性,并导致对治疗的耐药性[6]。此外,Tspyl5基因的表达还受到MUC16的调控,MUC16通过JAK2/STAT3/GR信号通路下调Tspyl5基因的表达,进而影响肿瘤的生长和化疗耐药性[7]。在乳腺癌中,Tspyl5基因的表达与患者的预后相关,低表达提示预后不良[8]。

综上所述,Tspyl5基因的表达和甲基化状态与多种癌症的发生、发展和治疗耐药性相关。Tspyl5基因可能作为一种潜在的肿瘤抑制基因,在肿瘤的发生和发展过程中发挥着重要作用。进一步研究Tspyl5基因的功能和调控机制,有助于深入理解肿瘤的发生和发展机制,为肿瘤的诊断、治疗和预后评估提供新的思路和策略。

参考文献:
1. Jung, Yeonjoo, Park, Jinah, Bang, Yung-Jue, Kim, Tae-You. 2007. Gene silencing of TSPYL5 mediated by aberrant promoter methylation in gastric cancers. In Laboratory investigation; a journal of technical methods and pathology, 88, 153-60. doi:. https://pubmed.ncbi.nlm.nih.gov/18059362/
2. Kumar, Senthil R, Bryan, Jeffrey N, Esebua, Magda, Amos-Landgraf, James, May, Tanner J. 2017. Testis specific Y-like 5: gene expression, methylation and implications for drug sensitivity in prostate carcinoma. In BMC cancer, 17, 158. doi:10.1186/s12885-017-3134-7. https://pubmed.ncbi.nlm.nih.gov/28235398/
3. Kim, Eun Jin, Lee, So Yong, Kim, Tae Rim, Kim, Kug Chan, Kim, In Gyu. 2010. TSPYL5 is involved in cell growth and the resistance to radiation in A549 cells via the regulation of p21(WAF1/Cip1) and PTEN/AKT pathway. In Biochemical and biophysical research communications, 392, 448-53. doi:10.1016/j.bbrc.2010.01.045. https://pubmed.ncbi.nlm.nih.gov/20079711/
4. Epping, Mirjam T, Meijer, Lars A T, Krijgsman, Oscar, Pandolfi, Pier Paolo, Bernards, René. 2010. TSPYL5 suppresses p53 levels and function by physical interaction with USP7. In Nature cell biology, 13, 102-8. doi:10.1038/ncb2142. https://pubmed.ncbi.nlm.nih.gov/21170034/
5. Huang, Chao, He, Chunping, Ruan, Peng, Zhou, Rui. 2020. TSPYL5 activates endoplasmic reticulum stress to inhibit cell proliferation, migration and invasion in colorectal cancer. In Oncology reports, 44, 449-456. doi:10.3892/or.2020.7639. https://pubmed.ncbi.nlm.nih.gov/32627024/
6. Kim, In-Gyu, Lee, Jei-Ha, Kim, Seo-Yeon, Kim, Rae-Kwon, Cho, Eun-Wie. 2021. Targeting therapy-resistant lung cancer stem cells via disruption of the AKT/TSPYL5/PTEN positive-feedback loop. In Communications biology, 4, 778. doi:10.1038/s42003-021-02303-x. https://pubmed.ncbi.nlm.nih.gov/34163000/
7. Leng, Xiangyou, Xie, Shengyu, Tao, Dachang, Liu, Yunqiang, Yang, Yuan. . Mouse Tspyl5 promotes spermatogonia proliferation through enhancing Pcna-mediated DNA replication. In Reproduction, fertility, and development, 36, . doi:10.1071/RD23042. https://pubmed.ncbi.nlm.nih.gov/38185096/
8. Lakshmanan, Imayavaramban, Salfity, Shereen, Seshacharyulu, Parthasarathy, Batra, Surinder K, Ganti, Apar Kishor. 2017. MUC16 Regulates TSPYL5 for Lung Cancer Cell Growth and Chemoresistance by Suppressing p53. In Clinical cancer research : an official journal of the American Association for Cancer Research, 23, 3906-3917. doi:10.1158/1078-0432.CCR-16-2530. https://pubmed.ncbi.nlm.nih.gov/28196872/