TRKC Effector Reporter Cell
CBP74500
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| I. Background | |
| TrkC(原肌球蛋白受體激酶 C)是神經(jīng)營養(yǎng)因子受體 Trk 家族的重要成員,由 NTRK3 基因編碼,作為一種受體酪氨酸激酶,它主要與其特異性配體神經(jīng)營養(yǎng)因子-3(NT-3)結(jié) 合,并在中樞和外周神經(jīng)系統(tǒng)的特定區(qū)域高表達(dá),尤其在與運(yùn)動(dòng)協(xié)調(diào)和平衡相關(guān)的本體感 覺神經(jīng)元以及小腦中發(fā)揮關(guān)鍵作用,主導(dǎo)神經(jīng)元的存活、分化與突觸可塑性。 NT-3/TRKC 信號通路是調(diào)控神經(jīng)系統(tǒng)發(fā)育與功能的核心通路,其中 NT-3 作為特異性 配體,與受體酪氨酸激酶 TRKC 結(jié)合后,誘導(dǎo)其發(fā)生二聚化及自磷酸化,從而激活下游 R AS/MAPK(增殖/分化)、PI3K/AKT(存活)和 PLC-γ(可塑性)三條關(guān)鍵信號級聯(lián),共 同介導(dǎo)神經(jīng)元的存活、分化、軸突生長及突觸可塑性,尤其對本體感覺等功能至關(guān)重要; 而該通路的病理激活源于 NTRK3 基因融合,導(dǎo)致 TRKC 激酶域發(fā)生配體非依賴性的持續(xù) 激活,進(jìn)而將這一維持神經(jīng)生存的生理通路轉(zhuǎn)化為驅(qū)動(dòng)多種癌癥的致癌引擎,成為廣譜靶 向藥物的作用基礎(chǔ)。 |
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| II. Description | |
TRKC Effector Reporter Cell 報(bào)告基因藥靶模型很好的模擬了體內(nèi) TRKC 的信號轉(zhuǎn)導(dǎo)過程,原理見下圖所示。![]() Figure 1. TRKC Effector Reporter Cell 模型原理圖 |
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| III. Introduction | |
| Expressed gene: | TRKC |
| 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 +2 μg/ml Puromycin+200 μg/ml Hygromycin B |
| Mycoplasma Testing: | Negative |
| Storage: | Liquid nitrogen |
| Application(s): | Functional(Report Gene) Assay |
| IV. Representative Data | |
![]() Figure 2. Recombinant TRKC Effector Reporter Cell stably expressing TRKC. ![]() Figure 3. Dose Response of Recombinant Human NT-3 in TRKC Effector Reporter Cell( C13). ![]() Figure 4. Dose Response of TRKC Agonist Ab in TRKC Effector Reporter Cell( C13). ![]() Figure 5. Inhibition of Human NT-3 induced Reporter Activity by NTRK Inhibitor in TRKC Effector Reporter Cell( C13). |
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