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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 CLEC5A Gene cDNA Clone (full-length ORF Clone), expression ready, FLAG-tagged||RG80259-G-F|
|Rat CLEC5A Gene cDNA Clone (full-length ORF Clone), expression ready, His-tagged||RG80259-G-H|
|Rat CLEC5A Gene cDNA Clone (full-length ORF Clone), expression ready, Myc-tagged||RG80259-G-M|
|Rat CLEC5A Gene cDNA Clone (full-length ORF Clone), expression ready, untagged||RG80259-G-N|
|Rat CLEC5A Gene cDNA Clone (full-length ORF Clone), expression ready, HA-tagged||RG80259-G-Y|
CLEC5A, also known as MDL1 and MDL-1, is a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Members of this family share a common protein fold and have diverse functions, such as cell adhesion, cell-cell signalling, glycoprotein turnover, and roles in inflammation and immune response. CLEC5A with dnax-activation protein 12 and may play a role in cell activation. It also functions as a positive regulator of osteoclastogenesis. CLEC5A acts as a key regulator of synovial injury and bone erosion during autoimmune joint inflammation .The binding of dengue virus to CLEC5A triggers signaling through the phosphylation of TYROBP, this interaction does not result in viral entry, but stimulates proinflammatory cytokine release.