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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.
|Mouse IL1R1 ORF mammalian expression plasmid, C-GFPSpark tag||MG50807-ACG|
|Mouse IL1R1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG50807-ACR|
|Mouse IL1R1 ORF mammalian expression plasmid, C-Flag tag||MG50807-CF|
|Mouse IL1R1 ORF mammalian expression plasmid, C-His tag||MG50807-CH|
|Mouse IL1R1 ORF mammalian expression plasmid, C-Myc tag||MG50807-CM|
|Mouse IL1R1 ORF mammalian expression plasmid, C-HA tag||MG50807-CY|
|Mouse IL1R1 ORF mammalian expression plasmid, N-Flag tag||MG50807-NF|
|Mouse IL1R1 ORF mammalian expression plasmid, N-His tag||MG50807-NH|
|Mouse IL1R1 ORF mammalian expression plasmid, N-Myc tag||MG50807-NM|
|Mouse IL1R1 ORF mammalian expression plasmid, N-HA tag||MG50807-NY|
|Mouse IL1R1 natural ORF mammalian expression plasmid||MG50807-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.