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.
|Canine IL18R1 ORF mammalian expression plasmid, C-Flag tag||DG70081-CF|
|Canine IL18R1 ORF mammalian expression plasmid, C-His tag||DG70081-CH|
|Canine IL18R1 ORF mammalian expression plasmid, C-Myc tag||DG70081-CM|
|Canine IL18R1 ORF mammalian expression plasmid, C-HA tag||DG70081-CY|
|Canine IL18R1 ORF mammalian expression plasmid, N-Flag tag||DG70081-NF|
|Canine IL18R1 ORF mammalian expression plasmid, N-His tag||DG70081-NH|
|Canine IL18R1 ORF mammalian expression plasmid, N-Myc tag||DG70081-NM|
|Canine IL18R1 ORF mammalian expression plasmid, N-HA tag||DG70081-NY|
|Canine IL18R1 natural ORF mammalian expression plasmid||DG70081-UT|
|Learn more about expression Vectors|
Interleukin-18 receptor 1 (IL18R1) also known as CD218 antigen-like family member A, CDw218a, IL1 receptor-related protein and CD218a, is an interleukin receptor of the immunoglobulin superfamily. IL18R1 is found expressed in lung, leukocytes, spleen, liver, thymus, prostate, small intestine, colon, placenta, and heart, and is absent from brain, skeletal muscle, pancreas, and kidney. High level of expression is found in Hodgkin disease cell lines. This receptor is specifically binds interleukin 18 (IL18), and is essential for IL18 mediated signal transduction. IL18R1 contains 3 Ig-like C2-type (immunoglobulin-like) domains and 1 TIR domain. It is a single-pass type I membrane protein. IFN-alpha and IL12 are reported to induce the expression of this receptor in NK and T cells. The increased expression of IL18R1 may contribute pathogenically to disease and is therefore a potential therapeutic target. The absence of a genetic association in the IL18R1 gene itself suggests regulation from other parts of the genome, or as part of the inflammatory cascade in multiple sclerosis without a prime genetic cause.