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pMD18-T Simple Vector is a high-efficiency TA cloning vector constructed from pUC18, of which the initial multiple cloning sites (MCS) were destroyed. Thus the cDNA should be amplified by PCR with primers containing a restriction site for subclone. Competent cells appropriate for pUC18 are also appropriated for the Vector, e.g. JM109, DH5α, TOP10. The pMD18-T Simple Vector is 2.6kb in size. Selection of the plasmid in E. coli is conferred by the ampicillin resistance gene. The coding sequence was inserted by TA cloning at site 425.
The coding sequence can be amplified by PCR with M13-47 and RV-M primers.
|Human C2 ORF mammalian expression plasmid, C-GFPSpark tag||HG10154-ACG|
|Human C2 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||HG10154-ACR|
|Human C2 ORF mammalian expression plasmid, C-Flag tag||HG10154-CF|
|Human C2 ORF mammalian expression plasmid, C-His tag||HG10154-CH|
|Human C2 ORF mammalian expression plasmid, C-Myc tag||HG10154-CM|
|Human C2 ORF mammalian expression plasmid, C-HA tag||HG10154-CY|
|Human C2 ORF mammalian expression plasmid, Flag tag||HG10154-M-F|
|Human C2 ORF mammalian expression plasmid, N-Flag tag||HG10154-NF|
|Human C2 ORF mammalian expression plasmid, N-His tag||HG10154-NH|
|Human C2 ORF mammalian expression plasmid, N-Myc tag||HG10154-NM|
|Human C2 ORF mammalian expression plasmid, N-HA tag||HG10154-NY|
|Human C2 natural ORF mammalian expression plasmid||HG10154-UT|
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Complement component C2 is part of the classical complement pathway which plays a major role in innate immunity against infection. C2 is a glycoprotein synthesized in liver hepatocytes and several other cell types in extrahepatic tissues. This pathway is triggered by a multimolecular complex C1, and subsequently the single-chain form of C2 is cleaved into two chains referred to C2a and C2b by activated C1. The second component of complement (C2) is a multi-domain serine protease that provides catalytic activity for the C3 and C5 convertases of the classical and lectin pathways of human complement. C4b and C2 was investigated by surface plasmon resonance. C2a containing a serine protease domain combines with complement component C4b to form the C3 convertase C4b2a which is responsible for C3 activation, and leads to the stimulation of adaptive immune responses via Lectin pathway. C2 bound to C4b is cleaved by classical (C1s) or lectin (MASP2) proteases to produce C4bC2a. C2 has the same serine protease domain as C4bC2a but in an inactive zymogen-like conformation, requiring cofactor-induced conformational change for activity. Deficiency of C2 (C2D) is the most common genetic deficiency of the complement system, and two types of C2D have been recognized in the context of specific MHC haplotypes. C2D in human is reported to increase susceptibility to infection, and is associated with certain autoimmune diseases, such as rheumatological disorders.