Ham's F-12K (Kaighn's) 培养基
Invitrogen17万+抗体限时买二赠一,靶点广,灵活用!
Ham's F-12K (Kaighn's) 培养基
Gibco™

Ham's F-12K (Kaighn's) 培养基

Ham's F-12K (Kaighn's) 培养基是 Ham's F-12 Nutrient Mixture 的改良产品。Ham's了解更多信息
Have Questions?
更改视图buttonViewtableView
货号数量
21127022500 mL
2112703010 x 500 mL
货号 21127022
价格(CNY)
440.80
飞享价
Ends: 31-Dec-2025
562.00
共减 121.20 (22%)
Each
添加至购物车
数量:
500 mL
Customize this product
价格(CNY)
440.80
飞享价
Ends: 31-Dec-2025
562.00
共减 121.20 (22%)
Each
添加至购物车
Ham's F-12K (Kaighn's) 培养基是 Ham's F-12 Nutrient Mixture 的改良产品。Ham's F-12K (Kaighn's) 培养基专门为原代人类肝细胞以及减血清环境中的部分大鼠和鸡肝细胞而开发。

这种 Ham's F-12K (Kaighn's) 培养基的生产方式如下:
包含不含
•L-谷氨酰胺•HEPES:
• 酚红

可提供完整配方

Ham's F-12K 的使用
Ham's F-12K (Kaighn's) 培养基含有传统基础培养基中不具备的多种成分,比如腐胺、胸苷、次黄嘌呤、锌以及较高水平的全部氨基酸和丙酮酸钠。添加这些成分后,对于某些细胞类型只需在培养基中补充极少量的血清或成分明确的组分。Ham's F-12K (Kaighn's) 培养基不含蛋白质或生长因子,因此通常会补充生长因子和胎牛血清 (FBS)。必须针对每种细胞系优化 FBS 浓度。Ham's F-12K (Kaighn's) 培养基使用碳酸氢钠缓冲体系 (2.5 g/L),因此需要 5–10% CO2 的环境来维持生理 pH 值。

两地 cGMP 生产
为确保供应链的稳定,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 Ham's F-12K (Kaighn's) 培养基。两个地点都符合 cGMP 生产要求,并通过 ISO 13485 认证,是在 FDA 登记的医疗器械生产商。
仅供科研使用。不可用于诊断程序。
规格
细胞类型人肝细胞
最大浓度1 X
生产质量cGMP-compliant under the ISO 13485 standard
产品线Gibco
产品类型Ham's F-12K (Kaighn's) 培养基
数量500 mL
有效期自生产之日起 12 个月
运输条件室温
分类非动物源性
形式液体
无菌无菌过滤
灭菌方法无菌过滤
加有添加剂低糖, 谷氨酰胺, 酚红, 丙酮酸钠
不加添加剂不含 HEPES
Unit SizeEach
内容与储存
储存条件:2-8°C。避光储存
运输条件:环境

常见问题解答 (FAQ)

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。

我的细胞不能贴附于培养容器。我该如何处理?

如果细胞经胰酶过度消化,即可能发生此种情况。尝试使用更短时间或更低浓度的胰酶进行消化处理。支原体污染也可能造成此种问题。分离部分细胞培养物,并检测支原体感染。最后,检查培养基中的粘附因子。

引用和文献 (5)

引用和文献
Abstract
Human MutY homolog, a DNA glycosylase involved in base excision repair, physically and functionally interacts with mismatch repair proteins human MutS homolog 2/human MutS homolog 6.
Authors: Gu Yesong; Parker Antony; Wilson Teresa M; Bai Haibo; Chang Dau-Yin; Lu A-Lien;
Journal:J Biol Chem
PubMed ID:11801590
Adenines mismatched with guanines or 7,8-dihydro-8-oxo-deoxyguanines that arise through DNA replication errors can be repaired by either base excision repair or mismatch repair. The human MutY homolog (hMYH), a DNA glycosylase, removes adenines from these mismatches. Human MutS homologs, hMSH2/hMSH6 (hMutSalpha), bind to the mismatches and initiate the repair on ... More
Stimulation of neuronal neurite outgrowth using functionalized carbon nanotubes.
Authors:Matsumoto K, Sato C, Naka Y, Whitby R, Shimizu N
Journal:Nanotechnology
PubMed ID:20173239
Low concentrations (0.11-1.7 microg ml(-1)) of functionalized carbon nanotubes (CNTs), which are multi-walled CNTs modified by amino groups, when added with nerve growth factor (NGF), promoted outgrowth of neuronal neurites in dorsal root ganglion (DRG) neurons and rat pheochromocytoma cell line PC12h cells in culture media. The quantity of active ... More
Dystrophin deficiency markedly increases enterovirus-induced cardiomyopathy: a genetic predisposition to viral heart disease.
Authors: Xiong Dingding; Lee Gil-Hwan; Badorff Cornel; Dorner Andrea; Lee Sang; Wolf Paul; Knowlton Kirk U;
Journal:Nat Med
PubMed ID:12118246
Both enteroviral infection of the heart and mutations in the dystrophin gene can cause cardiomyopathy. Little is known, however, about the interaction between genetic and acquired forms of cardiomyopathy. We previously demonstrated that the enteroviral protease 2A cleaves dystrophin; therefore, we hypothesized that dystrophin deficiency would predispose to enterovirus-induced cardiomyopathy. ... More
The Slp homology domain of synaptotagmin-like proteins 1-4 and Slac2 functions as a novel Rab27A binding domain.
Authors: Kuroda Taruho S; Fukuda Mitsunori; Ariga Hiroyoshi; Mikoshiba Katsuhiko;
Journal:J Biol Chem
PubMed ID:11773082
rab27A, which encodes a small GTP-binding protein, was recently identified as a gene in which mutations caused human hemophagocytic syndrome (Griscelli syndrome) and ashen mice, which exhibit defects in melanosome transport as well as in regulated granule exocytosis in cytotoxic T lymphocytes. However, little is known about the molecular mechanism ... More
Role for 18:1 lysophosphatidic acid as an autocrine mediator in prostate cancer cells.
Authors:Xie Y, Gibbs TC, Mukhin YV, Meier KE.
Journal:J Biol Chem
PubMed ID:12084719
Lysophosphatidic acid (LPA) is a lipid mediator that may play an important role in growth and survival of carcinomas. In this study, LPA production and response were characterized in two human prostate cancer (CaP) cell lines: PC-3 and Du145. Bombesin, a neuroendocrine peptide that is mitogenic for CaP cells, stimulated ... More