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.
|Rat IL1R1 ORF mammalian expression plasmid, C-GFPSpark tag||RG80028-ACG|
|Rat IL1R1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||RG80028-ACR|
|Rat IL1R1 ORF mammalian expression plasmid, C-Flag tag||RG80028-CF|
|Rat IL1R1 ORF mammalian expression plasmid, C-His tag||RG80028-CH|
|Rat IL1R1 ORF mammalian expression plasmid, C-Myc tag||RG80028-CM|
|Rat IL1R1 ORF mammalian expression plasmid, C-HA tag||RG80028-CY|
|Rat IL1R1 ORF mammalian expression plasmid, N-Flag tag||RG80028-NF|
|Rat IL1R1 ORF mammalian expression plasmid, N-His tag||RG80028-NH|
|Rat IL1R1 ORF mammalian expression plasmid, N-Myc tag||RG80028-NM|
|Rat IL1R1 ORF mammalian expression plasmid, N-HA tag||RG80028-NY|
|Rat IL1R1 natural ORF mammalian expression plasmid||RG80028-UT|
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Interleukin 1 receptor, type I (IL-1R1) also known as CD121a (Cluster of Differentiation 121a), is an interleukin receptor. IL-1R1/CD121a is a cytokine receptor that belongs to the interleukin 1 receptor family. This protein is a receptor for interleukin alpha (IL1A), interleukin beta (IL1B), and interleukin 1 receptor, type I (IL1R1/IL1RA). IL-1R1/CD121a is an important mediator involved in many cytokine induced immune and inflammatory responses. This protein has been characterized by pharmacological and molecular techniques in the mouse brain. The spindle-shaped astrocytes enclose the wound, separating the healthy from damaged neural tissue. The shape change and subsequent repair processes are IL-1β activity-dependent, acting through the IL-1 type 1 receptor (IL-1R1), as co-application of the IL-1type 1 receptor antagonist protein (IL-1ra) blocks IL-1β induced effects. In the spleen, a slight increase in IL-1R AcP and IL-1R1 was observed during the first hours following LPS stimulation. In conclusion, IL-1R AcP mRNA is expressed in the brain and in other tissues where IL-1R1/CD121a transcripts are found. However, the regulation of its expression is distinct from IL-1R1/CD121a. The high level of expression and the lack of regulation of IL-1R AcP transcripts in the brain under inflammatory conditions suggest that the protein might be constitutively expressed in excess.