IL6R KO STAT3-Luc HEK293
CBPB0021
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| I. Background | |
| 癌癥相關(guān)炎癥的特征是存在特定的炎癥細(xì)胞和炎癥介質(zhì),包括細(xì)胞因子和趨化因子。最近的證據(jù)表明,信號(hào)轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子(STAT)家族蛋白,特別是 STAT3,在惡性轉(zhuǎn)化開(kāi)始和癌癥進(jìn)展過(guò)程中,在選擇性誘導(dǎo)和維持癌前炎癥微環(huán)境中起著至關(guān)重要的作用。 信號(hào)轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子 3(STAT3)是一種轉(zhuǎn)錄激活因子,它將細(xì)胞外受體的信號(hào)直接傳遞到細(xì)胞核,介導(dǎo)一些基因的表達(dá),在細(xì)胞凋亡等細(xì)胞過(guò)程中發(fā)揮重要作用。在細(xì)胞因子和生長(zhǎng)因子的作用下,STAT3 被受體相關(guān) Janus 激酶(JAK)磷酸化,形成同二聚體或異二聚體,并轉(zhuǎn)位到細(xì)胞核中,作為轉(zhuǎn)錄激活劑發(fā)揮作用。STAT3 信號(hào)傳導(dǎo)是惡性腫瘤的主要內(nèi)在途徑,因?yàn)樗趷盒约?xì)胞中頻繁激活,并且在調(diào)節(jié)腫瘤微環(huán)境中對(duì)癌癥發(fā)炎至關(guān)重要的許多基因中起關(guān)鍵作用。 |
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| II. Description | |
IL6R KO STAT3-Luc HEK293 報(bào)告基因細(xì)胞,在 STAT3-Luc HEK293 細(xì)胞上敲除 IL6R。配體與 IL6R KO STAT3-Luc HEK293 結(jié)合,啟動(dòng) JAK/STAT3 信號(hào)通路,原理見(jiàn)下圖所示。![]() Figure 1. IL6R KO STAT3-Luc HEK293 細(xì)胞模型原理圖 |
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| III. Introduction | |
| 敲除基因: | IL6R |
| Expressed gene: | IL6R KO STAT3-Luc |
| Stability: | 32 passages (in-house test, that not means the cell line will be instable beyond the passages we tested.) |
| Freeze Medium: | 90% FBS+10% DMSO |
| Culture Medium: |
DMEM+10%FBS+100 μg/ml Hygromycin B
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| Mycoplasma Testing: | Negative |
| Storage: | Liquid nitrogen |
| IV. Description of Host Cell Line | |
| Organism: | Homo sapiens, human |
| Tissue: | Embryonic kidney |
| Disease: | Normal |
| Morphology: | Epithelial |
| Growth Properties: | Adherent |
| V. Representative Data | |
![]() Figure 2. Sanger of IL6R KO STAT3-Luc HEK293. ![]() Figure 3. Dose Response of Samples in IL6R KO STAT3-Luc HEK293(C15). ![]() Figure 4. Dose Response of Samples in IL6R KO STAT3-Luc HEK293(C15). |
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