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The pGEM-T is 3kb in length, and contains the amplicin resistance gene, conferring selection of the plasmid in E. coli, and the ori site which is the bacterial origin of replication. The plasmid has multiple cloning sites as shown below. The coding sequence was inserted by TA cloning. Many E. coli strains are suitable for the propagation of this vector including JM109, DH5α and TOP10.
The coding sequence can be easily obtained by digesting the vector with proper restriction enzyme(s). The coding sequence can also be amplified by PCR with M13 primers, or primer pair SP6 and T7.
|Rat SERPING1 ORF mammalian expression plasmid, C-GFPSpark tag||RG81647-ACG|
|Rat SERPING1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||RG81647-ACR|
|Rat SERPING1 ORF mammalian expression plasmid, C-Flag tag||RG81647-CF|
|Rat SERPING1 ORF mammalian expression plasmid, C-His tag||RG81647-CH|
|Rat SERPING1 ORF mammalian expression plasmid, C-Myc tag||RG81647-CM|
|Rat SERPING1 ORF mammalian expression plasmid, C-HA tag||RG81647-CY|
|Rat SERPING1 Gene cDNA clone plasmid||RG81647-G|
|Rat SERPING1 ORF mammalian expression plasmid, N-Flag tag||RG81647-NF|
|Rat SERPING1 ORF mammalian expression plasmid, N-His tag||RG81647-NH|
|Rat SERPING1 ORF mammalian expression plasmid, N-Myc tag||RG81647-NM|
|Rat SERPING1 ORF mammalian expression plasmid, N-HA tag||RG81647-NY|
|Rat SERPING1 natural ORF mammalian expression plasmid||RG81647-UT|
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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.