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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.
|Mouse MBL ORF mammalian expression plasmid, C-GFPSpark tag||MG50063-ACG|
|Mouse MBL ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG50063-ACR|
|Mouse MBL ORF mammalian expression plasmid, C-Flag tag||MG50063-CF|
|Mouse MBL ORF mammalian expression plasmid, C-His tag||MG50063-CH|
|Mouse MBL ORF mammalian expression plasmid, C-Myc tag||MG50063-CM|
|Mouse MBL ORF mammalian expression plasmid, C-HA tag||MG50063-CY|
|Mouse MBL ORF mammalian expression plasmid, N-Flag tag||MG50063-NF|
|Mouse MBL ORF mammalian expression plasmid, N-His tag||MG50063-NH|
|Mouse MBL ORF mammalian expression plasmid, N-Myc tag||MG50063-NM|
|Mouse MBL ORF mammalian expression plasmid, N-HA tag||MG50063-NY|
|Mouse MBL natural ORF mammalian expression plasmid||MG50063-UT|
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MBL (mannose-binding lectin) is primarily a liver-derived collagen-like serum protein, which binds sugar structures on micro-organisms and on dying host cells and is one of the four known mediators that initiate activation of the complement system via the lectin pathway. MBL and the ficolins (Ficolin-1, Ficolin-2 and Ficolin-3) are soluble collagen-like proteins that are involved in innate immune defence. They bind sugar structures or acetylated compounds present on microorganisms and on dying host cells and they initiate activation of the lectin complement pathway in varying degrees. MBL2 encodes the mannose-binding lectin, which is a key player in the innate immune system and has recently been found to play a role in development of type 1 diabetes and gestational diabetes mellitus. Common variant alleles situated both in promoter and structural regions of the MBL2 gene influence the stability and the serum concentration of the protein. Several polymorphisms in the promoter and structural regions of MBL2 adversely affect the plasma concentration and oligomeric state of MBL. The possession of mutant alleles has been linked to disease outcome for a variety of bacterial and viral infections. Mutant MBL2 haplotypes have been linked to disease progression and response to therapy in HCV infection.