|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
Human influenza hemagglutinin (HA) is a surface glycoprotein required for the infectivity of the human virus. The HA tag is derived from the HA-molecule corresponding to amino acids 98-106 has been extensively used as a general epitope tag in expression vectors. Many recombinant proteins have been engineered to express the HA tag, which does not appear to interfere with the bioactivity or the biodistribution of the recombinant protein. This tag facilitates the detection, isolation, and purification of the proteins.
The actual HA tag is as follows: 5' TAC CCA TAC GAT GTT CCA GAT TAC GCT 3' or 5' TAT CCA TAT GAT GTT CCA GAT TAT GCT 3' The amino acid sequence is: YPYDVPDYA.
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), C-GFPSpark 标签||HG10511-ACG|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), C-OFPSpark 标签||HG10511-ACR|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), C-Flag 标签||HG10511-CF|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), C-His 标签||HG10511-CH|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), C-Myc 标签||HG10511-CM|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), C-HA 标签||HG10511-CY|
|人 TREM-1/TREM1 基因ORF全长cDNA(克隆载体)||HG10511-M|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), N-Flag 标签||HG10511-NF|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), N-His 标签||HG10511-NH|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), N-Myc 标签||HG10511-NM|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体), N-HA 标签||HG10511-NY|
|人 TREM-1/TREM1 基因ORF全长cDNA克隆(表达载体)||HG10511-UT|
TREM1 (triggering receptor expressed on myeloid cells) is a type I transmembrane protein with a single Ig-like domain, and is selectively expressed on blood neutrophils and a subset of monocytes. As a member of the growing family of receptors related to NK cell receptors, TREM1 activates downstream signaling events with the help of an adapter protein called DAP12. Expression of TREM1 is up-regulated by bacterial LPS, a ligand for TLR4, as well as lipoteichoic acid. Although its natural ligand has not been identified, engagement of TREM1 with agonist mAbs triggers secretion of the proinflammatory cytokines TNF-α and IL-1β, as well as chemokines such as IL-8 and monocyte chemoattractant protein (MCP)-1. Intracellularly, TREM1 induces Ca2+ mobilization and tyrosine phosphorylation of extracellular signal-related kinase 1 (ERK1), ERK2 and phospholipase C-γ. In an animal model of LPS-induced septic shock, blockade of TREM1 signaling inhibited hyperresponsiveness and death. Thus, it has been demonstrated that TREM1 performs a critical function in immune responses involved in host defense against microbial challenges, and is suggested to be a potential therapeutic target for septic shock.