|Datasheet||Specific References||Reviews||Related Products||Protocols|
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.
|Cynomolgus monkey CLEC7A Gene cDNA Clone (full-length ORF Clone), expression ready, FLAG-tagged||CG90153-G-F|
|Cynomolgus monkey CLEC7A Gene cDNA Clone (full-length ORF Clone), expression ready, His-tagged||CG90153-G-H|
|Cynomolgus monkey CLEC7A Gene cDNA Clone (full-length ORF Clone), expression ready, Myc-tagged||CG90153-G-M|
|Cynomolgus monkey CLEC7A Gene cDNA Clone (full-length ORF Clone), expression ready, untagged||CG90153-G-N|
|Cynomolgus monkey CLEC7A Gene cDNA Clone (full-length ORF Clone), expression ready, HA-tagged||CG90153-G-Y|
Dectin-1 was recently identified as the most important receptor for beta-glucan. It is a type II transmembrane protein which binds beta-1,3 and beta-1,6 glucans, and is expressed on most cells of the innate immune system and has been implicated in phagocytosis as well as killing of fungi by macrophages, neutrophils and dendritic cells. Recognition of beta-glucan by dectin-1 triggers effective immune response, including phagocytosis and proinflammatory factor production, to eliminate infecting fungi, which especially benefits immunocompromised patients against opportunistic fungal infection. In addition, dectin-1 is involved in the adaptive immune response as well as autoimmune diseases and immune tolerance. Dectin-1 can recognize and respond to live fungal pathogens and is being increasingly appreciated as having a key role in the innate responses to these pathogens. In addition to its exogenous ligands, Dectin-1 can recognize an unidentified endogenous ligand on T cells and may act as a co-stimulatory molecule. Recent studies have highlighted the importance of Dectin-1 in anti-fungal immunity, in both mice and humans, and have suggested a possible involvement of this receptor in the control of mycobacterial infections.