CDKN1A基因敲除HCT116细胞
货号:
EDJ-KQ18757
物种:
人
细胞名称:
HCT 116
基因名称:
CDKN1A
基因ID:
1026
规格:
1×10⁶ cells
CDKN1A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-KQ18757 |
|---|---|
| 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 | CDKN1A |
| 基因ID | |
| 基因别名 | CAP20|CDKN1|CIP1|MDA-6|P21|SDI1|WAF1|p21CIP1 |
| 摘要 |
This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin-cyclin-dependent kinase2 or -cyclin-dependent kinase4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of this gene is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen, a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of cyclin-dependent kinase2, and may be instrumental in the execution of apoptosis following caspase activation. Mice that lack this gene have the ability to regenerate damaged or missing tissue. Multiple alternatively spliced variants have been found for this gene. [provided by RefSeq, Sep 2015]
|
| 癌症类型 | Colorectal Carcinoma |
| 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
野生型 p53 对 HSF1 活性的抑制为 p53 杂合性缺失创造了驱动力。
IF=15.7
Nature communications
肿瘤抑制因子 p53 通过 p21 - RB / E2F 信号传导和串联 E2F 位点下调 p107 ()。
IF=4.9
International journal of molecular sciences
该KO模型可能有助于:
- 研究p53介导的肿瘤抑制通路,包括p21-RB/E2F信号通路和转录调控。
- 研究p53和p107在细胞周期控制和肿瘤发生中的相互作用。
- 探索p21在野生型p53条件下调节HSF1活性的作用。
- 模拟p53杂合性缺失(LOH)的动态变化及其在癌症进展中的驱动力。
- 在结直肠癌背景下验证p21依赖的细胞凋亡或衰老机制的功能。