Opti-MEM™ 减血清培养基,粉末
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Opti-MEM™ 减血清培养基,粉末
Opti-MEM™ 减血清培养基,粉末
Opti-MEM™ 减血清培养基,粉末
Gibco™

Opti-MEM™ 减血清培养基,粉末

Opti-MEM™ 减血清培养基是一种经过改良的 Minimal Essential Medium (MEM),能够使胎牛血清添加量减少至少 50%,而生长速率或形态无变化。还推荐 Opti-MEM™ 与阳离子脂质体转染试剂了解更多信息
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货号数量
2260005010 x 1 L
2260013410 L
货号 22600050
价格(CNY)
4,579.00
Each
添加至购物车
数量:
10 x 1 L
Customize this product
价格(CNY)
4,579.00
Each
添加至购物车
Opti-MEM™ 减血清培养基是一种经过改良的 Minimal Essential Medium (MEM),能够使胎牛血清添加量减少至少 50%,而生长速率或形态无变化。还推荐 Opti-MEM™ 与阳离子脂质体转染试剂(如 Lipofectamine™ 试剂)配套使用。Opti-MEM™ 可用于各种悬浮和贴壁的哺乳动物细胞,包括 Sp2、AE-1、CHO、BHK-21、HEK 和原代成纤维细胞。针对广泛的细胞培养应用,提供了多种组分的 Gibco™ Opti-MEM™ 改良培养基。

这种 Opti-MEM™ 的改良方式如下:

包含
•L-谷氨酰胺
• 酚红

完整配方保密。有关更多信息,请联系技术服务部

Gibco™ Opti-MEM™ 是一种内含胰岛素、转铁蛋白、次黄嘌呤、胸苷和微量元素的独特培养基。这些附加组分可使血清添加量减少至少 50%。

cGMP 生产和质量体系
为确保供应链的稳定,我们同时在位于纽约格兰德岛和英国苏格兰的两家独立工厂生产 Gibco™ Opti-MEM™。两家工厂均符合 cGMP 生产要求,并通过 ISO 13485 认证,是在 FDA 注册的医疗器械生产商。

Gibco™ Opti-MEM™ 使用碳酸氢钠缓冲系统 (2.4 g/L),因此需要 5-10% CO2 环境来维持生理 pH 值。

粉末形式的 Gibco™ 细胞培养基在配制时需要补充碳酸氢钠、调节 pH 值并过滤(有关详细信息,参见方案)。
不可用于人类或动物的治疗。除产品用途之外的使用,可能违反当地法规。用于体外诊断。
规格
细胞系Sp2、AE-1、CHO、BHK-21 和 HEK
细胞类型原代成纤维细胞
生产质量cGMP-compliant under the ISO 13485 standard
产品线Gibco、Opti-MEM
产品类型Opti-MEM I
数量10 x 1 L
有效期自生产之日起 30 个月
运输条件室温
分类动物来源
形式粉末
无菌无菌过滤
加有添加剂谷氨酰胺, 酚红
Unit SizeEach
内容与储存
储存条件:2-8° C
运输条件:环境
有效期:自生产之日起30个月

常见问题解答 (FAQ)

我的粉末培养基一经溶解,其保质期有多久?

以干粉配制的液体培养基与相同配方的在售液体成品一样稳定。通常避光保存于4度冰箱可确保1个月的使用效果。

加入血清后的培养基可以使用多久?

通常情况下,加入血清后的培养基可使用三个星期。尽管没有正式的研究支持数据,这是我们研究人员的经验。

我的培养基是室温条件下运送来的,但注明应保存于冷藏条件下。这会有影响么?

我们会在常温下运输那些需要在冰箱中长期存放的培养基。我们对代表性的培养基配方进行了研究,结果表明这些培养基在室温下放置一周不会有问题。

我该如何去除细胞培养基中的支原体污染?

绝大部分情况下支原体污染无法从培养物中去除,只能弃用。不过也许您的培养物具有独特性,您不希望丢弃而试图去除污染。环丙沙星和Plasmocin据报导适合此种应用。如果对相关实验方案或应用感兴趣,请联系抗生素供应商或参考已发表的文献。请注意支原体很难从培养物中清除,而且容易扩散,所以请对受污染的培养物进行隔离处理,直至支原体被完全清除,另外您的实验室可能也需要彻底净化。

我发现培养物的生长速率变缓。我该如何处理?

尝试更换培养基或血清。比较培养基配方中葡萄糖、氨基酸及其他成份之间的差异。比较新旧批次的血清。增加细胞的初始接种量。最后,让细胞逐步切换到新的培养基。

引用和文献 (6)

引用和文献
Abstract
Folding of the striated muscle myosin motor domain.
Authors: Chow Diana; Srikakulam Rajani; Chen Ying; Winkelmann Donald A;
Journal:J Biol Chem
PubMed ID:12110670
'We have investigated the folding of the myosin motor domain using a chimera of an embryonic striated muscle myosin II motor domain fused on its COOH terminus to a thermal stable, fast folding variant of green fluorescent protein (GFP). In in vitro expression assays, the GFP domain of the chimeric ... More
Role of the E1A Rb-binding domain in repression of the NF-kappa B-dependent defense against tumor necrosis factor-alpha.
Authors: Cook James L; Walker Thomas A; Worthen G Scott; Radke Jay R;
Journal:Proc Natl Acad Sci U S A
PubMed ID:12119420
'The adenoviral E1A oncogene sensitizes mammalian cells to tumor necrosis factor-alpha (TNF-alpha), in part by repressing the nuclear factor-kappa B (NF-kappa B)-dependent defense against this cytokine. Other E1A activities involve binding to either p300/cyclic AMP response element-binding protein (CBP) or retinoblastoma (Rb)-family proteins, but the roles of E1A interactions with ... More
Induction of bacterial lipoprotein tolerance is associated with suppression of toll-like receptor 2 expression.
Authors:Wang JH, Doyle M, Manning BJ, Di Wu Q, Blankson S, Redmond HP.
Journal:J Biol Chem
PubMed ID:12133836
'Tolerance to bacterial cell wall components including lipopolysaccharide (LPS) may represent an essential regulatory mechanism during bacterial infection. Two members of the Toll-like receptor (TLR) family, TLR2 and TLR4, recognize the specific pattern of bacterial cell wall components. TLR4 has been found to be responsible for LPS tolerance. However, the ... More
Hepatitis C virus subgenomic replicons in the human embryonic kidney 293 cell line.
Authors:Ali S, Pellerin C, Lamarre D, Kukolj G,
Journal:J Virol
PubMed ID:14671129
'Hepatitis C virus (HCV) infects liver cells and its replication in other cells is incompletely defined. Human hepatoma Huh-7 cells harboring subgenomic HCV replicons were used in somatic cell fusion experiments with human embryonic kidney 293 cells as a means of examining the permissiveness of 293 cells for HCV subgenomic ... More
c-Myc sensitizes cells to tumor necrosis factor-mediated apoptosis by inhibiting nuclear factor kappa B transactivation.
Authors: You Zongbing; Madrid Lee V; Saims Daniel; Sedivy John; Wang Cun-Yu;
Journal:J Biol Chem
PubMed ID:12149248
Nuclear factor kappaB (NF-kappaB) plays a key role in suppression of tumor necrosis factor (TNF)-mediated apoptosis by inducing a variety of anti-apoptotic genes. Expression of c-Myc has been shown to sensitize cells to TNF-mediated apoptosis by inhibiting NF-kappaB activation. However, the precise step in the NF-kappaB signaling pathway and apoptosis ... More