RNF144B基因敲除HEK293细胞
货号:
EDJ-KQ11802
物种:
人
细胞名称:
HEK293
基因名称:
RNF144B
基因ID:
255488
规格:
1×10⁶cells
RNF144B基因敲除细胞HEK293是由艾迪基因优化的CRISPR/Cas9编辑而成，采用Sanger测序法验证敲除，保证单克隆，活性良好。
| 货号 | EDJ-KQ11802 |
|---|---|
| 产品名称 | RNF144B Knockout HEK293 Cell Line |
| 细胞 | HEK293 |
| Cellosaurus ID | CVCL_0045 |
| 细胞别名 | Hek293, HEK-293, HEK/293, (HEK)293, HEK 293, HEK,293, 293, 293 HEK, 293 Ad5, Graham 293, Graham-293, Human Embryonic Kidney 293 |
| 基因 | RNF144B |
| 基因ID | |
| 基因别名 | IBRDC2|PIR2|bA528A10.3|p53RFP |
| 摘要 |
Enables ubiquitin-protein transferase activity. Involved in negative regulation of apoptotic process and ubiquitin-dependent protein catabolic process. Located in mitochondrial membrane. [provided by Alliance of Genome Resources, Jul 2025]
|
| 癌症类型 | Non-tumor |
| 细胞形态 | Adherent |
| 传代比率 | 1/2~1/4 |
| 完全培养基 | DMEM + 10% FBS |
| 冻存培养基 | 95%完全培养基+ 5% DMSO |
* 仅供科研使用，不适用于人体或动物，包括临床、治疗或诊断用途。
| Loci | 送检细胞STR信息 送检细胞名: HEK293 | 细胞库细胞STR信息 细胞库细胞名: HEK293 | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | X | ||
| CSF1P0 | 12 | 11 | 12 | |
| D2S1338 | 19 | 19 | ||
| D3S1358 | 15 | 17 | 15 | 17 |
| D5S818 | 8 | 8 | 9 | |
| D7S820 | 11 | 12 | 11 | 12 |
| D8S1179 | 12 | 14 | 12 | 14 |
| D13S317 | 12 | 14 | 12 | 14 |
| D16S539 | 9 | 13 | 9 | 13 |
| D18S51 | 17 | 18 | 17 | 18 |
| D19S433 | 15 | 18 | 15 | 18 |
| D21S11 | 28 | 30.2 | 28 | 30.2 |
| FGA | 23 | 23 | ||
| Penta D | 9 | 10 | 9 | 10 |
| Penta E | 7 | 15 | 7 | 15 |
| TH01 | 7 | 9.3 | 7 | 9.3 |
| TPOX | 11 | 11 | ||
| vWA | 16 | 19 | 16 | 19 |
| D6S1043 | 11 | 11 | ||
| D12S391 | 19 | 21 | 11 | 15 |
| D2S441 | 11 | 15 | 11 | 15 |
* 该细胞系与收录于ATCC, DSMZ, JCRB 和 RIKEN数据库的细胞系STR数据匹配。
结论：该细胞 STR 鉴定正确。
结论：该细胞 STR 鉴定正确。
* 研究用途免责声明：本内容基于公开的研究数据、生物信息学资源及计算分析生成，仅供研究参考。
相关研究文献
RNF144B 通过靶向 MDA5 进行自噬降解来负调控抗病毒免疫。
IF=6.2
EMBO reports
As a RIG-I-like receptor, MDA5 plays a critical role in antiviral innate immunity by acting as a cytoplasmic double-stranded RNA sensor capable of initiating type I interferon pathways. Here, we show that RNF144B specifically interacts with MDA5 and promotes K27/K33-linked polyubiquitination of MDA5 at lysine 23 and lysine 43, which promotes autophagic degradation of MDA5 by p62. Rnf144b deficiency greatly promotes IFN production and inhibits EMCV replication in vivo. Importantly, Rnf144b mice has a significantly higher overall survival rate than wild-type mice upon EMCV infection. Collectively, our results identify RNF144B as a negative regulator of innate antiviral response by targeting CARDs of MDA5 and mediating autophagic degradation of MDA5.
该敲除模型可用于：
- 研究RNF144B在负调节先天抗病毒免疫中的作用。
- 研究MDA5介导的信号通路和自噬降解机制。
- 验证RNF144B作为抗病毒免疫调节靶点的功能。
- 探索病毒感染模型中RNF144B依赖性自噬。
- 筛选调节RNF144B-MDA5轴活性的化合物。
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