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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 VCAM1 ORF mammalian expression plasmid, C-GFPSpark tag||RG80233-ACG|
|Rat VCAM1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||RG80233-ACR|
|Rat VCAM1 ORF mammalian expression plasmid, C-Flag tag||RG80233-CF|
|Rat VCAM1 ORF mammalian expression plasmid, C-His tag||RG80233-CH|
|Rat VCAM1 ORF mammalian expression plasmid, C-Myc tag||RG80233-CM|
|Rat VCAM1 ORF mammalian expression plasmid, C-HA tag||RG80233-CY|
|Rat VCAM1 ORF mammalian expression plasmid, N-Flag tag||RG80233-NF|
|Rat VCAM1 ORF mammalian expression plasmid, N-His tag||RG80233-NH|
|Rat VCAM1 ORF mammalian expression plasmid, N-Myc tag||RG80233-NM|
|Rat VCAM1 ORF mammalian expression plasmid, N-HA tag||RG80233-NY|
|Rat VCAM1 natural ORF mammalian expression plasmid||RG80233-UT|
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Vascular cell adhesion molecule 1 (VCAM-1), also known as CD106, is a cell surface sialoglycoprotein belonging to the immunoglobulin superfamily. Two forms of VCAM-1 with either six or seven extracellular Ig-like domains are generated by alternative splicing, with the longer form predominant. VCAM-1 is an endothelial ligand for very late antigen-4 (VLA-4) and α4ß7 integrin expressed on leukocytes, and thus mediates leukocyte-endothelial cell adhesion and signal transduction. VCAM-1 expression is induced on endothelial cells during inflammatory bowel disease, atherosclerosis, allograft rejection, infection, and asthmatic responses. During these responses, VCAM-1 forms a scaffold for leukocyte migration. VCAM-1 also activates signals within endothelial cells resulting in the opening of an "endothelial cell gate" through which leukocytes migrate. VCAM-1 has been identified as a potential anti-inflammatory therapeutic target, the hypothesis being that reduced expression of VCAM-1 will slow the development of atherosclerosis. In addition, VCAM-1-activated signals in endothelial cells are regulated by cytokines indicating that it is important to consider both endothelial cell adhesion molecule expression and function during inflammatory processes.