C2orf48基因敲除HCT116细胞
货号:
EDJ-KQ71329
物种:
人
细胞名称:
HCT 116
基因名称:
RRM2
基因ID:
6241
规格:
1×10⁶ cells
C2orf48基因敲除细胞HCT116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-KQ71329 |
|---|---|
| 细胞 | HCT116 |
| Cellosaurus ID | CVCL_0291 |
| 细胞别名 | HCT-116, HCT.116, HCT_116, HCT116, HCT116wt, HCT-116/P, HCT-116/parental, CoCL2 |
| 基因 | C2orf48 |
| 基因ID | |
| 摘要 |
This gene encodes one of two non-identical subunits for ribonucleotide reductase. This reductase catalyzes the formation of deoxyribonucleotides from ribonucleotides. Synthesis of the encoded protein (M2) is regulated in a cell-cycle dependent fashion. Transcription from this gene can initiate from alternative promoters, which results in two isoforms that differ in the lengths of their N-termini. Related pseudogenes have been identified on chromosomes 1 and X. [provided by RefSeq, Sep 2009]
|
| 细胞形态 | Adherent |
| 传代比率 | 1/5-1/4,2days |
| 完全培养基 | mcCoy5A+10% FBS |
| 冻存培养基 | 90% FBS/完培+10% 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: HCT 116 | 细胞库细胞STR信息 细胞库细胞名: HCT 116 | ||||||
| Allele1 | Allele2 | Allele3 | Allele4 | Allele1 | Allele2 | Allele3 | Allele4 | |
| Amelogenin | X | X | ||||||
| CSF1PO | 7 | 10 | 7 | 9 | 10 | 11 | ||
| D2S1338 | 16 | 16 | ||||||
| D3S1358 | 12 | 17 | 18 | 19 | 12 | 18 | 19 | |
| D5S818 | 10 | 11 | 10 | 11 | ||||
| D7S820 | 11 | 12 | 11 | 12 | ||||
| D8S1179 | 10 | 12 | 14 | 15 | 10 | 12 | 14 | 15 |
| D13S317 | 10 | 12 | 10 | 12 | ||||
| D16S539 | 11 | 13 | 11 | 12 | 13 | 14 | ||
| D18S51 | 16 | 17 | 16 | 17 | ||||
| D19S433 | 12 | 13 | 12 | |||||
| D21S11 | 29 | 30 | 29 | 30 | ||||
| FGA | 18 | 23 | 18 | 23 | ||||
| Penta D | 9 | 13 | 9 | 13 | ||||
| Penta E | 12 | 13 | 14 | 12 | 13 | 14 | ||
| TH01 | 8 | 9 | 8 | 9 | ||||
| TPOX | 8 | 8 | ||||||
| vWA | 17 | 21 | 22 | 23 | 17 | 21 | 22 | 23 |
| D6S1043 | 13 | |||||||
| D12S391 | 17 | 21 | 22 | |||||
| D2S441 | 11 | 12 | ||||||
* 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
p53 缺陷通过上调 RRM2 并通过下调 SIRT7 使 RRM2 巴豆酰化来介导顺铂耐药。
IF=4
Frontiers in molecular biosciences
该KO模型可能有助于:
- 研究p53介导的RRM2在化疗耐药中的调控作用;
- 研究RRM2巴豆酰化和SIRT7在DNA损伤修复通路中的作用;
- 顺铂敏感性和耐药机制的药物筛选;
- RRM2在核苷酸代谢和细胞周期调控中的功能分析;
- 与p53依赖性和非依赖性细胞死亡通路相关的凋亡检测。