PTEN基因敲除A549细胞
货号:
EDJ-KQ62744
物种:
人
细胞名称:
A-549
基因名称:
PTEN
基因ID:
5728
规格:
1×10⁶cells
PTEN基因敲除细胞A549是由EVO视讯 EVO真人生命基因优化的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-KQ62744 |
|---|---|
| 产品名称 | PTEN 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 | PTEN |
| 基因ID |
5728
|
| 基因别名 | 10q23del|BZS|CWS1|DEC|GLM2|MHAM|MMAC1|PTEN1|PTENbeta|PTENgama|TEP1 |
| 摘要 |
This gene was identified as a tumor suppressor that is mutated in a large number of cancers at high frequency. The protein encoded by this gene is a phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase. It contains a tensin like domain as well as a catalytic domain similar to that of the dual specificity protein tyrosine phosphatases. Unlike most of the protein tyrosine phosphatases, this protein preferentially dephosphorylates phosphoinositide substrates. It negatively regulates intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells and functions as a tumor suppressor by negatively regulating AKT/PKB signaling pathway. The use of a non-canonical (CUG) upstream initiation site produces a longer isoform that initiates translation with a leucine, and is thought to be preferentially associated with the mitochondrial inner membrane. This longer isoform may help regulate energy metabolism in the mitochondria. A pseudogene of this gene is found on chromosome 9. Alternative splicing and the use of multiple translation start codons results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Feb 2015]
|
| 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。
相关文献
PINK1诱导丝氨酸442处丝裂原融合蛋白2的磷酸化导致其蛋白酶体降解并促进肺癌和肺动脉高压中的细胞增殖。
IF=4.2
FASEB journal : official publication of the Federation of American Societies for Experimental Biolog
MicroRNA-25-3p促进顺铂耐药性在非小细胞肺癌(NSCLC)顺利获得调整PTEN / PI3K / AKT途径。
IF=4.2
Bioengineered
该KO模型可能有助于:
- 研究非小细胞肺癌(NSCLC)耐药性中的PTEN/PI3K/AKT信号通路;
- 评估顺铂耐药机制及潜在的逆转策略;
- 研究肺癌中的线粒体动力学和线粒体自噬通路;
- 对PTEN缺失在细胞增殖和存活实验中的功能进行分析;
- 筛选靶向PTEN依赖性凋亡或代谢脆弱性的治疗药物。