SMARCA4基因敲除HEK293细胞
货号:
EDJ-KQ15359
物种:
人
细胞名称:
HEK293
基因名称:
SMARCA4
基因ID:
6597
规格:
1×10⁶cells
SMARCA4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-KQ15359 |
|---|---|
| 产品名称 | SMARCA4 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 | SMARCA4 |
| 基因ID | |
| 基因别名 | BAF190|BAF190A|BRG1|CSS4|MRD16|OTSC12|RTPS2|SNF2|SNF2-beta|SNF2L4|SNF2LB|SWI2|hSNF2b |
| 摘要 |
The protein encoded by this gene is a member of the SWI/SNF family of proteins and is similar to the brahma protein of Drosophila. Members of this family have helicase and ATPase activities and are thought to regulate transcription of certain genes by altering the chromatin structure around those genes. The encoded protein is part of the large ATP-dependent chromatin remodeling complex SNF/SWI, which is required for transcriptional activation of genes normally repressed by chromatin. In addition, this protein can bind BRCA1, as well as regulate the expression of the tumorigenic protein CD44. Mutations in this gene cause rhabdoid tumor predisposition syndrome type 2. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, May 2012]
|
| 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
SMARCA4 / 2 缺失通过限制 IP3R3 介导的 Ca 流向线粒体来抑制化疗诱导的细胞凋亡。
IF=15.7
Nature communications
Inactivating mutations in SMARCA4 and concurrent epigenetic silencing of SMARCA2 characterize subsets of ovarian and lung cancers. Concomitant loss of these key subunits of SWI/SNF chromatin remodeling complexes in both cancers is associated with chemotherapy resistance and poor prognosis. Here, we discover that SMARCA4/2 loss inhibits chemotherapy-induced apoptosis through disrupting intracellular organelle calcium ion (Ca) release in these cancers. By restricting chromatin accessibility to ITPR3, encoding Ca channel IP3R3, SMARCA4/2 deficiency causes reduced IP3R3 expression leading to impaired Ca transfer from the endoplasmic reticulum to mitochondria required for apoptosis induction. Reactivation of SMARCA2 by a histone deacetylase inhibitor rescues IP3R3 expression and enhances cisplatin response in SMARCA4/2-deficient cancer cells both in vitro and in vivo. Our findings elucidate the contribution of SMARCA4/2 to Ca-dependent apoptosis induction, which may be exploited to enhance chemotherapy response in SMARCA4/2-deficient cancers.
该敲除模型可用于：
- 研究SMARCA4在化疗诱导凋亡中的作用。
- 研究IP3R3介导的从内质网到线粒体的钙通量。
- 探索癌症药物治疗中的耐药机制。
- 验证SMARCA4/2缺失在线粒体信号通路中的功能。
- 筛选在SMARCA4缺陷细胞中恢复凋亡的化合物。
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