Ddias-KO 基因敲除小鼠

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产品名称

Ddias-KO 基因敲除小鼠

产品编号

S-KO-14262

品系全称

C57BL/6JCya-Ddiasem1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-74041-Ddias-B6J-VA

品系状态

使用本品系发表的文献需注明: Ddias-KO 基因敲除小鼠 mice (Strain S-KO-14262) 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
DNA damage-induced apoptosis suppressor
基因别称
4632434I11Rik,noxin
染色体号
Chr 7 (Mouse)
转录本 ID
NCBI: NM_001355126 | Ensembl: ENSMUST00000032877
修饰方式
全身性基因敲除
靶向范围
Exon 3~6
敲除长度
~9.8 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:1921291Mice homozygous for a null allele show an enlarged heart, several altered hematopoietic parameters, decreased number of spermatids, and increased cell death and increased cell sensitivity to induced-stress.
DDIAS,全称为DNA损伤诱导的凋亡抑制因子,是一种在DNA损伤反应中发挥关键作用的蛋白质。它主要通过抑制细胞凋亡来促进细胞的存活,从而在癌症的发生和发展中扮演重要角色。DDIAS在多种类型的癌症中都有表达,包括肺癌、肝细胞癌和胶质瘤等。研究表明,DDIAS的表达水平与癌症的侵袭性、增殖能力和预后密切相关。此外,DDIAS还与化疗耐药性相关,例如在肺癌细胞中,DDIAS的表达上调会导致对顺铂的耐药性。

研究表明,DDIAS的表达受多种信号通路的调控,包括NFATc1、ERK5/MEF2B和STAT3等。NFATc1是一种转录因子,可以激活DDIAS的转录,从而提高DDIAS的表达水平。ERK5/MEF2B信号通路也可以激活DDIAS的转录,而STAT3信号通路则与DDIAS的相互作用有关。DDIAS与STAT3的相互作用可以促进STAT3的酪氨酸磷酸化,进而激活STAT3信号通路,促进癌细胞的生存和增殖。

此外,DDIAS的表达还与多种细胞因子和生长因子有关。例如,EGF可以激活ERK5/MEF2B信号通路,进而提高DDIAS的表达水平。DDIAS的表达还与HSP70/CHIP信号通路有关,CHIP可以促进DDIAS的泛素化降解,从而降低DDIAS的表达水平。

在急性髓系白血病(AML)患者中,DDIAS的表达水平与预后不良相关。DDIAS的表达可以抑制AML细胞的凋亡,从而促进AML的发生和发展。此外,DDIAS的表达还与AML细胞的侵袭性和增殖能力相关。

研究表明,DDIAS的表达水平与肺癌患者的预后不良相关。DDIAS的表达可以促进肺癌细胞的侵袭性和增殖能力,从而促进肺癌的发生和发展。此外,DDIAS的表达还与肺癌细胞的化疗耐药性相关。

研究表明,DDIAS的表达水平与胶质瘤的发生和发展密切相关。DDIAS的表达可以促进胶质瘤细胞的侵袭性和增殖能力,从而促进胶质瘤的发生和发展。此外,DDIAS的表达还与胶质瘤细胞的干性相关。

研究表明,机械拉伸可以抑制人原发性气道基底干细胞的增殖和分化,并促进其凋亡。DDIAS是机械拉伸条件下人原发性气道基底干细胞中表达下调的基因之一。这表明,DDIAS可能在气道基底干细胞的增殖、分化和凋亡中发挥重要作用。

综上所述,DDIAS是一种在癌症的发生和发展中发挥重要作用的蛋白质。DDIAS的表达受多种信号通路的调控,包括NFATc1、ERK5/MEF2B和STAT3等。DDIAS的表达与多种癌症的侵袭性、增殖能力和预后密切相关。此外,DDIAS的表达还与化疗耐药性和干性相关。因此,DDIAS可能成为癌症治疗的新靶点[1,2,3,4,5,6,7,8,9,10]。

参考文献:
1. Im, Joo-Young, Kim, Bo-Kyung, Yoon, Sung-Hoon, Gong, Young-Dae, Won, Misun. 2021. DGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway. In Experimental & molecular medicine, 53, 643-653. doi:10.1038/s12276-021-00601-2. https://pubmed.ncbi.nlm.nih.gov/33859351/
2. Liu, Nan, Zhang, Xiupeng, Zhou, Haijing, Qiu, Xueshan, Wang, Enhua. 2017. DDIAS promotes invasion and proliferation of non-small cell lung cancer and predicts poor survival of lung cancer patients. In International journal of clinical and experimental pathology, 10, 11506-11515. doi:. https://pubmed.ncbi.nlm.nih.gov/31966506/
3. Im, Joo-Young, Lee, Kang-Woo, Won, Kyoung-Jae, Song, Kyung-Bin, Won, Misun. 2015. DNA damage-induced apoptosis suppressor (DDIAS), a novel target of NFATc1, is associated with cisplatin resistance in lung cancer. In Biochimica et biophysica acta, 1863, 40-9. doi:10.1016/j.bbamcr.2015.10.011. https://pubmed.ncbi.nlm.nih.gov/26493727/
4. Im, Joo-Young, Yoon, Sung-Hoon, Kim, Bo-Kyung, Jung, Kyeong Eun, Won, Misun. 2016. DNA damage induced apoptosis suppressor (DDIAS) is upregulated via ERK5/MEF2B signaling and promotes β-catenin-mediated invasion. In Biochimica et biophysica acta, 1859, 1449-1458. doi:10.1016/j.bbagrm.2016.07.003. https://pubmed.ncbi.nlm.nih.gov/27412911/
5. Naghinezhad, Jalal, Alenabi, Anita, Ayatollahi, Hossein, Khoshnegah, Zahra, Boroumand-Noughabi, Samaneh. 2023. Expression of DR4, DR5, FAS, Caspase-8 and, DDIAS Genes in AML Patients. In Medical journal of the Islamic Republic of Iran, 37, 68. doi:10.47176/mjiri.37.68. https://pubmed.ncbi.nlm.nih.gov/37575689/
6. Chen, You Lin, Liu, Yi, Xu, Yan, Su, Hong Wei, Liao, Li Shang. 2024. DNA Damage-Induced Apoptosis Suppressor Triggers Progression and Stemness of Glioma by Enhancing Lymphoid Enhancer-Binding Factor 1 Expression. In World journal of oncology, 15, 209-222. doi:10.14740/wjon1754. https://pubmed.ncbi.nlm.nih.gov/38545470/
7. Won, Kyoung-Jae, Im, Joo-Young, Kim, Bo-Kyung, Jung, Kyeong Eun, Won, Misun. 2017. Stability of the cancer target DDIAS is regulated by the CHIP/HSP70 pathway in lung cancer cells. In Cell death & disease, 8, e2554. doi:10.1038/cddis.2016.488. https://pubmed.ncbi.nlm.nih.gov/28079882/
8. Yoon, Sung-Hoon, Kim, Bo-Kyung, Kang, Mi-Jung, Im, Joo-Young, Won, Misun. 2020. Miconazole inhibits signal transducer and activator of transcription 3 signaling by preventing its interaction with DNA damage-induced apoptosis suppressor. In Cancer science, 111, 2499-2507. doi:10.1111/cas.14432. https://pubmed.ncbi.nlm.nih.gov/32476221/
9. Brunette, Gregory J, Jamalruddin, Mohd A, Baldock, Robert A, Clark, Nathan L, Bernstein, Kara A. 2019. Evolution-based screening enables genome-wide prioritization and discovery of DNA repair genes. In Proceedings of the National Academy of Sciences of the United States of America, 116, 19593-19599. doi:10.1073/pnas.1906559116. https://pubmed.ncbi.nlm.nih.gov/31501324/
10. Lin, Li-Qin, Zeng, Hai-Kang, Luo, Yu-Long, Wu, Hong-Kai, Li, Shi-Yue. 2023. Mechanical stretch promotes apoptosis and impedes ciliogenesis of primary human airway basal stem cells. In Respiratory research, 24, 237. doi:10.1186/s12931-023-02528-w. https://pubmed.ncbi.nlm.nih.gov/37773064/