|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.
|Human SERPING1 ORF mammalian expression plasmid, C-GFPSpark tag||HG10995-ACG|
|Human SERPING1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||HG10995-ACR|
|Human SERPING1 ORF mammalian expression plasmid, C-Flag tag||HG10995-CF|
|Human SERPING1 ORF mammalian expression plasmid, C-His tag||HG10995-CH|
|Human SERPING1 ORF mammalian expression plasmid, C-Myc tag||HG10995-CM|
|Human SERPING1 ORF mammalian expression plasmid, C-HA tag||HG10995-CY|
|Human SERPING1 Gene cDNA clone plasmid||HG10995-M|
|Human SERPING1 natural ORF mammalian expression plasmid||HG10995-M-N|
|Human SERPING1 ORF mammalian expression plasmid, N-Flag tag||HG10995-NF|
|Human SERPING1 ORF mammalian expression plasmid, N-His tag||HG10995-NH|
|Human SERPING1 ORF mammalian expression plasmid, N-Myc tag||HG10995-NM|
|Human SERPING1 ORF mammalian expression plasmid, N-HA tag||HG10995-NY|
|Human SERPING1 natural ORF mammalian expression plasmid||HG10995-UT|
|Learn more about expression Vectors|
Plasma protease C1 inhibitor, also known as C1-inhibiting factor, C1-INH, C1 esterase inhibitor, SERPING1 and C1IN, is a serine proteinase inhibitor (serpin) that regulates activation of both the complement and contact systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases. The N-terminal end (nonserpin domain) confers to C1-INH the capacity to bind lipopolysaccharides and E-selectin. Owing to this moiety, C1-INH intervenes in regulation of the inflammatory reaction. The heterozygous deficiency of C1-INH results in hereditary angioedema (HAE). Owing to its ability to modulate the contact and complement systems and the convincing safety profile, plasma-derived C1 inhibitor is an attractive therapeutic protein to treat inflammatory diseases other than HAE. Deficiency of C1 inhibitor results in hereditary angioedema, which is characterized by recurrent episodes of localized angioedema of the skin, gastrointestinal mucosa or upper respiratory mucosa. C1 inhibitor may prove useful in a variety of other diseases including septic shock, reperfusion injury, hyperacute transplant rejection, traumatic and hemorrhagic shock, and the increased vascular permeability associated with thermal injury, interleukin-2 therapy and cardiopulmonary bypass.