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产品目录
  • 细胞培养进口血清
    进口胎牛血清
    进口新生牛血清
    进口猪血清
    马血清
  • 支原体检测盒及标准品
    常规PCR检测试剂盒
    荧光定量PCR检测（qPCR法）
    支原体DNA提取
    灵敏度标准品（方法验证用）
    特异性标准品（方法验证用）
    PCR定量标准品（可用于方法验证）
  • 支原体祛除试剂
    细胞中支原体祛除
    环境支原体祛除
    水槽支原体祛除
  • 干细胞培养基
  • DNA/RNA污染祛除
    DNA/RNA污染祛除试剂
    DNA污染监测
  • RNA病毒研究试剂
    RNA病毒检测试剂盒
    病毒RNA提取
  • PCR仪器及配套产品
    DNA污染监测祛除
    PCR/qPCR仪性能检查
    PCR试剂
    PCR试剂盒
    PCR预混液（冻干粉）
    热启动聚合酶MB Taq DNA
  • 微生物PCR检测
    食品检测类产品
    食品微生物检测
    细菌PCR检测

胎牛血清的热灭活内毒素污染影响人类T淋巴细胞蛋白质组和磷酸化

2016-10-11 14:35

目前的研究提供了新的信息关于FCS热失活的影响和改变FCS-LPS浓度在细胞蛋白表达,并在人类T淋巴母翻译修饰。热失活和有限合伙人污染FCS的调节蛋白质的表达和磷酸化参与基本细胞功能,如蛋白质合成、细胞骨架稳定性、氧化应激调控和细胞凋亡。因此,研究强调需要考虑热失活和有限合伙人FCS的污染因素可以影响T淋巴母细胞蛋白质组。

英文原文：

Fetal calf serum heat inactivation and lipopolysaccharide contamination influence the human T lymphoblast proteome and phosphoproteome

Background

The effects of fetal calf serum (FCS) heat inactivation and bacterial lipopolysaccharide (LPS) contamination on cell physiology have been studied, but their effect on the proteome of cultured cells has yet to be described. This study was undertaken to investigate the effects of heat inactivation of FCS and LPS contamination on the human T lymphoblast proteome. Human T lymphoblastic leukaemia (CCRF-CEM) cells were grown in FCS, either non-heated, or heat inactivated, having low (< 1 EU/mL) or regular (< 30 EU/mL) LPS concentrations. Protein lysates were resolved by 2-DE followed by phospho-specific and silver nitrate staining. Differentially regulated spots were identified by nano LC ESI Q-TOF MS/MS analysis.

Results

A total of four proteins (EIF3M, PRS7, PSB4, and SNAPA) were up-regulated when CCRF-CEM cells were grown in media supplemented with heat inactivated FCS (HE) as compared to cells grown in media with non-heated FCS (NHE). Six proteins (TCPD, ACTA, NACA, TCTP, ACTB, and ICLN) displayed a differential phosphorylation pattern between the NHE and HE groups. Compared to the low concentration LPS group, regular levels of LPS resulted in the up-regulation of three proteins (SYBF, QCR1, and SUCB1).

Conclusion