STAT2基因敲除A549细胞
货号:
EDJ-KQ18900
物种:
人
细胞名称:
A-549
基因名称:
STAT2
基因ID:
6773
规格:
1×10⁶cells
STAT2基因敲除细胞A549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-KQ18900 |
|---|---|
| 产品名称 | STAT2 Knockout A549 Cell Line |
| 细胞 | A549 |
| Cellosaurus ID | CVCL_0023 |
| 细胞别名 | A 549, A549, NCI-A549, A549/ATCC, A549 ATCC, A549ATCC, hA549 |
| 基因 | STAT2 |
| 基因ID | |
| 基因别名 | IMD44|ISGF-3|P113|PTORCH3|STAT113 |
| 摘要 |
The protein encoded by this gene is a member of the STAT protein family. In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators. In response to interferon (IFN), this protein forms a complex with STAT1 and IFN regulatory factor family protein p48 (ISGF3G), in which this protein acts as a transactivator, but lacks the ability to bind DNA directly. The protein mediates innate antiviral activity. Mutations in this gene result in Immunodeficiency 44. [provided by RefSeq, Aug 2020]
|
| 癌症类型 | Non-Small Cell Lung Carcinoma |
| 细胞形态 | Adherent |
| 传代比率 | 1/5-1/4 ,2days |
| 完全培养基 | F-12K + 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: A-549 | 细胞库细胞STR信息 细胞库细胞名: A-549 | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | Y | X | Y |
| CSF1PO | 10 | 12 | 10 | 12 |
| D2S1338 | 24 | 24 | ||
| D3S1358 | 16 | 16 | ||
| D5S818 | 11 | 11 | ||
| D7S820 | 8 | 11 | 8 | 11 |
| D8S1179 | 13 | 14 | 13 | 14 |
| D13S317 | 11 | 11 | ||
| D16S539 | 11 | 12 | 11 | 12 |
| D18S51 | 14 | 17 | 14 | 17 |
| D19S433 | 13 | 13 | ||
| D21S11 | 29 | 29 | ||
| FGA | 23 | 23 | ||
| Penta D | 9 | 9 | ||
| Penta E | 7 | 11 | 7 | 11 |
| TH01 | 8 | 9.3 | 8 | 9.3 |
| TPOX | 8 | 11 | 8 | 11 |
| vWA | 14 | 14 | ||
| D6S1043 | 11 | 13 | ||
| D12S391 | 18 | 18 | ||
| D2S441 | 10 | 13 | 10 | 13 |
* 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。
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该KO模型可能有助于:
- 研究寨卡病毒和登革热病毒等黄病毒逃避I型干扰素信号传导的机制;
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- 评估涉及NS5介导的STAT2降解和免疫基因抑制的宿主-病毒相互作用;
- 验证调节STAT2稳定性或信号传导的抗病毒药物靶点的功能;
- 筛选在STAT2缺陷细胞环境中恢复干扰素信号传导的化合物。