TLR4基因敲除HEK293细胞
货号:
EDJ-KQ1491
物种:
人
细胞名称:
HEK293
基因名称:
TLR4
基因ID:
7099
规格:
1×10⁶cells
TLR4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-KQ1491 |
|---|---|
| 产品名称 | TLR4 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 | TLR4 |
| 基因ID | |
| 基因别名 | ARMD10|CD284|TLR-4|TOLL |
| 摘要 |
The protein encoded by this gene is a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize pathogen-associated molecular patterns that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity. The various TLRs exhibit different patterns of expression. In silico studies have found a particularly strong binding of surface TLR4 with the spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of Coronavirus disease-2019 (COVID-19). This receptor has also been implicated in signal transduction events induced by lipopolysaccharide (LPS) found in most gram-negative bacteria. Mutations in this gene have been associated with differences in LPS responsiveness, and with susceptibility to age-related macular degeneration. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2020]
|
| 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
LPS 通过细胞内 TLR4 - PI3K 信号传导加剧 TRPV4 介导的瘙痒。
IF=4.2
Journal of cellular and molecular medicine
Pruritus is often accompanied with bacterial infections, but the underlying mechanism is not fully understood. Although previous studies revealed that lipopolysaccharides (LPS) could directly activate TRPV4 channel and TRPV4 is involved in the generation of both acute itch and chronic itch, whether and how LPS affects TRPV4-mediated itch sensation remains unclear. Here, we showed that LPS-mediated TRPV4 sensitization exacerbated GSK101-induced scratching behaviour in mice. Moreover, this effect was compromised in TLR4-knockout mice, suggesting LPS acted through a TLR4-dependent mechanism. Mechanistically, LPS enhanced GSK101-evoked calcium influx in mouse ear skin cells and HEK293T cells transfected with TRPV4. Further, LPS sensitized TRPV4 channel through the intracellular TLR4-PI3K-AKT signalling. In summary, our study found a modulatory role of LPS in TRPV4 function and highlighted the TLR4-TRPV4 interaction in itch signal amplification.
该敲除模型可用于:
- 研究细胞内 TLR4-PI3K-AKT 信号在 TRPV4 通道敏化和钙内流中的作用
- 研究 LPS 加剧 TRPV4 介导的急慢性瘙痒的机制
- 解析 TLR4 依赖的感觉神经元和皮肤细胞中 TRPV4 功能调节
- 评估 TLR4-TRPV4 相互作用作为细菌感染相关瘙痒信号放大的靶点
- 验证 TLR4 在 LPS 诱导的 GSK101 诱发搔抓行为增强中的特异性贡献