TM4SF5基因敲除HEK293细胞

TM4SF5基因敲除HEK293细胞
货号:

EDJ-KQ6439

物种:

细胞名称:

HEK293

基因名称:

TM4SF5

基因ID:

9032

规格:

1×10⁶cells

TM4SF5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-KQ6439
产品名称 TM4SF5 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 TM4SF5
基因ID
基因别名 -
摘要
The protein encoded by this gene is a member of the transmembrane 4 superfamily, also known as the tetraspanin family. Most of these members are cell-surface proteins that are characterized by the presence of four hydrophobic domains. The proteins mediate signal transduction events that play a role in the regulation of cell development, activation, growth and motility. This encoded protein is a cell surface glycoprotein and is highly similar in sequence and structure to transmembrane 4 superfamily member 1. It may play a role in cell proliferation, and overexpression of this protein may be associated with the uncontrolled growth of tumour cells. [provided by RefSeq, Jul 2008]
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
Archives of biochemistry and biophysics
Transmembrane 4 L six family member 5 (TM4SF5) is involved in nonalcoholic steatosis and further aggravation of liver disease. However, its mechanism for regulating FA accumulation is unknown. We investigated how TM4SF5 in hepatocytes affected FA accumulation during acute FA supply. TM4SF5-expressing hepatocytes and mouse livers accumulated less FAs, compared with those of TM4SF5 deficiency or inactivation. Binding of TM4SF5 to SLC27A2 increased gradually upon acute FA treatment, whereas TM4SF5 constitutively bound SLC27A5. Suppression of either SLC27A2 or SLC27A5 in hepatocytes expressing TM4SF5 differentially modulated initial and maximal FA uptake levels for a fast turnover of fatty acid. Altogether, TM4SF5 negatively modulates FA accumulation into hepatocytes via association with the transporters for an energy homeostasis, when FA are supplied acutely.
该敲除模型可用于: - 研究TM4SF5在肝脏脂肪酸摄取和脂质代谢中的作用。 - 研究急性脂肪酸供应条件下TM4SF5与SLC27A转运蛋白的调节相互作用。 - 探索TM4SF5介导的信号通路在代谢应激反应中的作用。 - 验证TM4SF5作为肝细胞脂质稳态调节剂的功能。 - 筛选靶向TM4SF5依赖性代谢途径的化合物。

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