( We provide with BID qPCR primers for gene expression analysis, HP100042 )
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive ,Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A polyhistidine-tag is an amino acid motif in proteins that consists of at least five histidine (His) residues, often at the N- or C-terminus of the protein.
Polyhistidine-tags are often used for affinity purification of polyhistidine-tagged recombinant proteins expressed in Escherichia coli and other prokarfyotic expression systems.
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), C-GFPSpark 标签||HG10468-ACG|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), C-OFPSpark 标签||HG10468-ACR|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), N-GFPSpark 标签||HG10468-ANG|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), N-OFPSpark 标签||HG10468-ANR|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), C-Flag 标签||HG10468-CF|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), C-His 标签||HG10468-CH|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), C-Myc 标签||HG10468-CM|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), C-HA 标签||HG10468-CY|
|人 p22 BID 基因ORF全长cDNA(克隆载体)||HG10468-M|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体)||HG10468-M-N|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), N-Flag 标签||HG10468-NF|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), N-His 标签||HG10468-NH|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), N-Myc 标签||HG10468-NM|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体), N-HA 标签||HG10468-NY|
|人 p22 BID 基因ORF全长cDNA克隆(表达载体)||HG10468-UT|
The BH3 interacting domain death agonist (BID) is a pro-apoptotic member of the Bcl-2 protein family, which contains only the BH3 domain, and is required for its interaction with the Bcl-2 family proteins and for its pro-death activity. BID is important to cell death mediated by these proteases and thus is the sentinel to protease-mediated death signals. Recent studies further indicate that Bid may be more than just a killer molecule, it could be also involved in the maintenance of genomic stability by engaging at mitosis checkpoint. BID is an integrating key regulator of the intrinsic death pathway that amplifies caspase-dependent and caspase-independent execution of neuronal apoptosis. Therefore pharmacological inhibition of BID provides a promising therapeutic strategy in neurological diseases where programmed cell death is prominent. BID is activated by Caspase 8 in response to Fas/TNF-R1 death receptor activation. Activated BID is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. BID action has been proposed to involve the mitochondrial re-location of its truncated form, tBid, to facilitate the release of apoptogenic proteins like cytochrome c.