|Datasheet||Specific References||Reviews||Related Products||Protocols|
|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.
|Rat TNFRSF14 ORF mammalian expression plasmid, C-GFPSpark tag||RG80449-ACG|
|Rat TNFRSF14 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||RG80449-ACR|
|Rat TNFRSF14 ORF mammalian expression plasmid, C-Flag tag||RG80449-CF|
|Rat TNFRSF14 ORF mammalian expression plasmid, C-His tag||RG80449-CH|
|Rat TNFRSF14 ORF mammalian expression plasmid, C-Myc tag||RG80449-CM|
|Rat TNFRSF14 ORF mammalian expression plasmid, C-HA tag||RG80449-CY|
|Rat TNFRSF14 Gene cDNA clone plasmid||RG80449-G|
|Rat TNFRSF14 ORF mammalian expression plasmid, N-Flag tag||RG80449-NF|
|Rat TNFRSF14 ORF mammalian expression plasmid, N-His tag||RG80449-NH|
|Rat TNFRSF14 ORF mammalian expression plasmid, N-Myc tag||RG80449-NM|
|Rat TNFRSF14 ORF mammalian expression plasmid, N-HA tag||RG80449-NY|
|Rat TNFRSF14 natural ORF mammalian expression plasmid||RG80449-UT|
|Learn more about expression Vectors|
Herpesvirus entry mediator (HVEM), also referred to as TNFRSF14, TR2 (TNF receptor-like molecule) and ATAR (another TRAF-associated receptor), is a member of type I transmembrane protein belonging to the TNF-receptor superfamily. It is expressed on many immune cells, including T and B cells, NK cells, monocytes, and neutrophils. Two TNF superfamily ligands lymphotoxin α (TNF-β) and LIGHT (TNFSF14) are identified as cellular ligands for HVEM and initiate the positive signaling. However, recent studies have revealed that HVEM is also involved in the unique inhibitory signaling pathway for T cells through activating tyrosine phosphorylation of the immunoreceptor tyrosine-based inhibitory motif (ITIM) in B and T lymphocyte attenuator (BTLA). HVEM provides a stimulatory signal following engagement with LIGHT (TNFSF14) on T cells. In contrast, it can also provide an inhibitory signal to T cells when it binds the B and T lymphocyte attenuator (BTLA), a ligand member of the Immunoglobulin (Ig) superfamily. Thus, HVEM may be viewed as a molecular switch, capable of facilitating both stimulatory and inhibitory cosignaling in T cells. Substantial evidence from both human disease and from experimental mouse models has indicated that dysregulation of the LIGHT-HVEM-BTLA cosignaling pathway can cause inflammation in the lung and in mucosal tissues.