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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.
|Human C7 Gene cDNA Clone (full-length ORF Clone), expression ready, FLAG-tagged||HG13848-G-F|
|Human C7 Gene cDNA Clone (full-length ORF Clone), expression ready, His-tagged||HG13848-G-H|
|Human C7 Gene cDNA Clone (full-length ORF Clone), expression ready, Myc-tagged||HG13848-G-M|
|Human C7 Gene cDNA Clone (full-length ORF Clone), expression ready, untagged||HG13848-G-N|
|Human C7 Gene cDNA Clone (full-length ORF Clone), expression ready, HA-tagged||HG13848-G-Y|
Complement component 7 is a component of the complement system. It belongs to the complement C6/C7/C8/C9 family. It contains 1 EGF-like domain, 1 LDL-receptor class A domain, 1 MACPF domain, 2 Sushi (CCP/SCR) domains and 2 TSP type-1 domains. Complement component 7 serves as a membrane anchor. It participates in the formation of Membrane Attack Complex (MAC). People with C7 deficiency are prone to bacterial infection. It is a constituent of MAC that plays a key role in the innate and adaptive immune response by forming pores in the plasma membrane of target cells. Defects in C7 are a cause of complement component 7 deficiency (C7D). A rare defect of the complement classical pathway associated with susceptibility to severe recurrent infections, predominantly by Neisseria gonorrhoeae or Neisseria meningitidis.