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產品名稱:HCT8/L人結腸癌耐細胞株、HCT8/L人結腸癌耐細胞株、HCT8/L人結腸癌耐細胞株、HCT8/L人結腸癌耐細胞株;
細胞系特征 | ||
編號:MXC508 細胞株名稱:HCT8/L人結腸癌耐細胞株 種屬:人 組織來源:結腸癌 生長特性:貼壁生長 形態(tài)特征:上皮細胞 微生物及支原體檢測:陰性 安全性:所有腫瘤和病毒轉染的細胞均視為有潛在的生物危害性,必須在二級生物安全臺內操作,并請注意防護,所有廢液及接觸過此細胞的器皿需高壓滅菌后方能丟棄。 | ||
培養(yǎng)條件:
| 培養(yǎng)基:90%RPMI-1640+10%胎牛血清+1000ng/ml 血清我們推薦用: GIBCOFBS-10099-141或HYCLONEFBS-SH30084.03。 培養(yǎng)條件:37.0C carbon dioxide(CO2),5% | |
傳代方法:
| 收到細胞后,在倒置鏡下(是在4X物鏡)觀察整個細胞生長情況。 (一)如果細胞未長滿,用75%酒精噴灑整個瓶消毒后放到超菌臺內,嚴格無菌操作,打開細胞培養(yǎng)瓶,吸出培養(yǎng)液,換 10ml新鮮培養(yǎng)液后繼續(xù)培養(yǎng)。 (二)如果細胞已長滿,即可進行傳代培養(yǎng)。具體步驟如下: 1. 棄去培養(yǎng)液,用PBS(不含鈣,鎂離子)洗1-2次。 2. 加0.7-1ml消化液(0.25%Trypsin-0.53mM EDTA)于培養(yǎng)瓶中,用力拍打瓶壁,期間每隔 5-10s放到顯微鏡下觀察,直至50-70%的細胞脫落后,加入2ml 以上培養(yǎng)基中止消化。 3. 按6-8ml/瓶補加培養(yǎng)基,輕輕打勻后吸出一半,分到新的培養(yǎng)瓶中。如果沒有特別說明,收到細胞后的次傳代一般是一傳二。 注:1、觀察細胞在低倍鏡(4或5X物鏡)下進行,否則不能準確判斷細胞的傳代密度??醇毎男螒B(tài)請在10X或20X物鏡下。 2、瓶中運輸培養(yǎng)基不能重復再用,請換用加雙抗的新培養(yǎng)基,細胞凍存后,培養(yǎng)基中可不加任何抗生素。 3、有些細胞貼壁不牢,如發(fā)現(xiàn)貼壁細胞有脫落,可離心吹打后接種到新瓶內。 4、收到細胞后,若發(fā)現(xiàn)培養(yǎng)瓶破損、有液溢出及細胞有污染,請及時與我們聯(lián)系。..
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凍存方法: | 凍存液:90%胎牛血清,10%DMSO 儲存:液氮儲存 |
ATP per molecule of glucose than mitochondrial oxidative phosphorylation, is increasedat a time when expectedly T cells would require more efficient metabolism to meet a large energetic and biosynthetic demands to sustain cell proliferation and cytokine production. The purpose of increased glycolytic activity remains to be fully elucidated, but likely extends beyond that of merely providing ATP or even carbon for biosynthesis, as glucose does not contribute to most of carbon in proliferating T cells [ 12]. It has been proposed that glycolysis may be
In addition to the regulation of T cell activation and tolerance, T cell metabolism has also
compared to regulatory T cells (Tregs), which have increased rates of lipid oxidation [21]. These characteristics do not merely represent metabolic profiles of Teffs versus Tregs, but they actively determine differentiation and polarization. For example, Th17-polarizing
conditions have been shown to induce expression of glycolytic enzymes and to increase
glycolytic activity, while inhibition of glycolysis reciprocally reduces generation of Th17 cells and promotes Treg differentiation [22]. Mechanistically, glycolysis, and likewise
glutaminolysis, may drive Th17 differentiation at least in part by limiting the availability of fructose-6-phosphate to the hexosamine/N-glycan branching pathways, which leads to
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