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描述
For research or for further manufacturing use.
质量水平
无菌性
sterile-filtered
形式
liquid
储存条件
protect from light
技术
cell culture | mammalian: suitable
组分
L-glutamine: no
运输
ambient
储存温度
2-8°C
应用
Claycomb培养基是以建立HL-1细胞系的William Claycomb博士命名的，它专用于培养小鼠心肌细胞生长。HL-1是第一个能够在 体外维持分化心肌细胞表型和收缩活性的细胞系。HL-1细胞系可用于研究心肌梗塞后的心肌细胞肥大、测试新型心脏治疗药物和疗法、生产高水平心肌蛋白以及研究成熟心肌细胞特异性基因。补充100 μM去甲肾上腺素、10％胎牛血清（FBS）和4mM L-谷氨酰胺的Claycomb培养基，将能够维持HL-1细胞系和成熟心肌细胞的行为。在光学显微镜下观察HL-1细胞时，可以观察到细胞个体和群体的收缩随心肌细胞逐渐融合而变得更加频繁。
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产品编号
说明
价格
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
常规特殊物品
动植物来源培养基
Jan Hendrik van Weerd et al.
eLife, 9 (2020-07-17)
Genome-wide association studies have implicated common genomic variants in the gene desert upstream of TBX3 in cardiac conduction velocity. Whether these noncoding variants affect expression of TBX3 or neighboring genes and how they affect cardiac conduction is not understood. Here
L A Sikkink et al.
Cell death & disease, 1, e98-e98 (2010-01-01)
Light-chain amyloidosis (AL) is a devastating protein-misfolding disease characterized by abnormal proliferation of plasma cells in the bone marrow that secrete monoclonal immunoglobulin light chains that misfold and form amyloid fibrils, thus causing organ failure and death. Numerous reports on
Ivana Poparic et al.
PloS one, 6(10), e26524-e26524 (2011-11-05)
Four-and-a-half LIM domain protein 1 isoform A (FHL1A) is predominantly expressed in skeletal and cardiac muscle. Mutations in the FHL1 gene are causative for several types of hereditary myopathies including X-linked myopathy with postural muscle atrophy (XMPMA). We here studied
Malou van den Boogaard et al.
Cell reports, 28(10), 2704-2714 (2019-09-05)
The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential. Mutations in KCNH2 that cause a reduction of the repolarizing current can result in cardiac arrhythmias
Yunchang Liu et al.
Cell death & disease, 11(9), 756-756 (2020-09-17)
In this study, we first established the doxorubicin-induced cardiotoxicity (DIC) model with C57BL/6 mice and confirmed cardiac dysfunction with transthoracic echocardiography examination. RNA-sequencing was then performed to explore the potential mechanisms and transcriptional changes in the process. The metabolic pathway
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