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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.
|Mouse IL7R ORF mammalian expression plasmid, C-GFPSpark tag||MG50090-ACG|
|Mouse IL7R ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG50090-ACR|
|Mouse IL7R ORF mammalian expression plasmid, C-Flag tag||MG50090-CF|
|Mouse IL7R ORF mammalian expression plasmid, C-His tag||MG50090-CH|
|Mouse IL7R ORF mammalian expression plasmid, C-Myc tag||MG50090-CM|
|Mouse IL7R ORF mammalian expression plasmid, C-HA tag||MG50090-CY|
|Mouse IL7R ORF mammalian expression plasmid, N-Flag tag||MG50090-NF|
|Mouse IL7R ORF mammalian expression plasmid, N-His tag||MG50090-NH|
|Mouse IL7R ORF mammalian expression plasmid, N-Myc tag||MG50090-NM|
|Mouse IL7R ORF mammalian expression plasmid, N-HA tag||MG50090-NY|
|Mouse IL7R natural ORF mammalian expression plasmid||MG50090-UT|
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Interleukin 7 Receptor alpha (IL-7RA), also known as CD127, is a 75 kDa hematopoietin receptor superfamily member that plays an important role in lymphocyte differentiation, proliferation, and survival. IL-7 receptor alpha (CD127) signaling is essential for T-cell development and regulation of naive and memory T-cell homeostasis. IL-7RA is critically required for the proper development and function of lymphoid cells. Therefore, the IL-7RA is critically required for the proper development and function of lymphoid cells. Studies from both pathogenic and controlled HIV infection indicate that the containment of immune activation and preservation of CD127 expression are critical to the stability of CD4(+) T cells in infection. A better understanding of the factors regulating CD127 expression in HIV disease, particularly on T(CM) cells, might unveil new approaches exploiting the IL-7/IL-7R receptor pathway to restore T cell homeostasis and promote immune reconstitution in HIV infection. Factors relevant to HIV infection that could potentially decrease CD127 expression on human CD8(+) T cells. CD127 down-regulation may be an important contributor to HIV-associated T-cell dysfunction. In addition to IL-7, IL-7RA also associates with TSLPR to form the functional receptor for thymic stromal lymphopoietin (TSLP) which indirectly regulates T cell development by modulating dendritic cell activation. Mutations in the human IL-7RA gene cause a type of severe combined immunodeficiency in which the major deficiencies are in T cell development, whereas B and NK cells are relatively normal in number. Variation in the IL7RA gene was recently found associated with multiple sclerosis (MS). The polymorphisms in the IL7RA gene is involved in MS pathogenesis and suggest that IL7RA variation may primarily affect chronic disease courses. Soluble CD127 (sCD127) appears to play an important role in the immunopathogenesis of several chronic infections, multiple sclerosis, and various cancers.