产品中心 / 产品类型 / 细胞系&裂解液 / KO细胞裂解液

CASP8 Knockout HeLa Cell Lysate, Homozygous (RM02001)

Genome sequence analysis of PCR products from parental (WT) and CASP8 knockout (KO) HeLa cells, using sanger sequencing.

All(1)|
货号: RM02001
促销价:   ¥4700
抗体定制服务咨询

文献引用 (0)

详细信息

靶点
CASP8
细胞系
HeLa
突变描述
CASP8 Knockout HeLa Cell Line is engineered from HeLa cell line with Gene-Editing technology.
Allele-1:118bp deletion in exon1
Allele-2:118bp deletion in exon1

Mammalian cells such as human, rat and mouse cells are normally diploid with two alleles.
Homozygote: both alleles were knocked out, mRNA has no signal, no expression of proteins.
Heterozygote: only one allele was knocked out, the mRNA transcript levels was decreased compared to wild type, and the protein expression levels was also lower than that of the wild type.
敲除验证
Sanger Sequencing
产品组成
1 vial parental cell Lysate and 1 vial knockout cell Lysate
裂解液量
50μL, 2μg/μL.
使用方法
To be used as WB control. Lysate is supplied in 1× SDS sample buffer (2% SDS, 60 mM
Tris-HCl pH 6.8, 10% Glycerol, 0.02% Bromophenol blue, 60 mM beta-mercaptoethanol).
Lysate should be boiled for 3 - 5 minutes before loading onto gel.
物种
Human
保存条件
Lysate is stable for 12 months when stored at -20℃. Minimizing freeze-thaw cycles.
运输条件
4℃

背景信息

This gene encodes a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes composed of a prodomain, a large protease subunit, and a small protease subunit. Activation of caspases requires proteolytic processing at conserved internal aspartic residues to generate a heterodimeric enzyme consisting of the large and small subunits. This protein is involved in the programmed cell death induced by Fas and various apoptotic stimuli. The N-terminal FADD-like death effector domain of this protein suggests that it may interact with Fas-interacting protein FADD. This protein was detected in the insoluble fraction of the affected brain region from Huntington disease patients but not in those from normal controls, which implicated the role in neurodegenerative diseases. Many alternatively spliced transcript variants encoding different isoforms have been described, although not all variants have had their full-length sequences determined. [provided by RefSeq, Jul 2008]

>