SRI基因敲除HEK293细胞

SRI基因敲除HEK293细胞
货号:

EDJ-KQ5838

物种:

细胞名称:

HEK293

基因名称:

SRI

基因ID:

6717

规格:

1×10⁶cells

SRI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-KQ5838
产品名称 SRI 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 SRI
基因ID
基因别名 CP-22|CP22|SCN|V19
摘要
This gene encodes a calcium-binding protein with multiple E-F hand domains that relocates from the cytoplasm to the sarcoplasmic reticulum in response to elevated calcium levels. In addition to regulating intracellular calcium homeostasis it also modulates excitation-contraction coupling in the heart. Alternative splicing results in multiple transcript variants encoding distinct proteins. Multiple pseudogenes exist for this gene. [provided by RefSeq, Mar 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
Allele1Allele2Allele1 Allele2
AmelogeninXX
CSF1P0121112
D2S13381919
D3S135815171517
D5S818889
D7S82011121112
D8S117912141214
D13S31712141214
D16S539913913
D18S5117181718
D19S43315181518
D21S112830.22830.2
FGA2323
Penta D910910
Penta E715715
TH0179.379.3
TPOX1111
vWA16191619
D6S10431111
D12S39119211115
D2S44111151115
* 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。
* 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

IF=3
FEBS letters
Sorcin is a calcium-binding protein involved in maintaining endoplasmic reticulum (ER) Ca stores. We have previously shown that overexpressing sorcin under the rat insulin promoter was protective against high-fat diet-induced pancreatic beta-cell dysfunction in vivo. Activating transcription factor 6 (ATF6) is a key mediator of the unfolded protein response (UPR) that provides cellular protection during the progression of ER stress. Here, using nonexcitable HEK293 cells, we show that sorcin overexpression increased ATF6 signalling, whereas sorcin knock out caused a reduction in ATF6 transcriptional activity and increased ER stress. Altogether, our data suggest that sorcin downregulation during lipotoxic stress may prevent full ATF6 activation and a normal UPR during the progression of obesity and insulin resistance.
该敲除模型可用于: - 研究sorcin通过ATF6转录活性调节未折叠蛋白反应的作用。 - 研究钙结合蛋白在内质网应激信号通路中的功能。 - 探索钙稳态与UPR激活之间的相互作用。 - 验证sorcin作为应激诱导基因表达调节剂的功能。 - 在sorcin缺乏背景下筛选调节ATF6依赖性UPR的化合物。

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