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.
|Rhesus IFNB1 ORF mammalian expression plasmid, C-GFPSpark tag||CG90104-ACG|
|Rhesus IFNB1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||CG90104-ACR|
|Rhesus IFNB1 ORF mammalian expression plasmid, C-Flag tag||CG90104-CF|
|Rhesus IFNB1 ORF mammalian expression plasmid, C-His tag||CG90104-CH|
|Rhesus IFNB1 ORF mammalian expression plasmid, C-Myc tag||CG90104-CM|
|Rhesus IFNB1 ORF mammalian expression plasmid, C-HA tag||CG90104-CY|
|Rhesus IFNB1 ORF mammalian expression plasmid, N-Flag tag||CG90104-NF|
|Rhesus IFNB1 ORF mammalian expression plasmid, N-His tag||CG90104-NH|
|Rhesus IFNB1 ORF mammalian expression plasmid, N-Myc tag||CG90104-NM|
|Rhesus IFNB1 ORF mammalian expression plasmid, N-HA tag||CG90104-NY|
|Rhesus IFNB1 natural ORF mammalian expression plasmid||CG90104-UT|
|Learn more about expression Vectors|
Interferons (IFNs) are natural glycoproteins belonging to the cytokine superfamily, and are produced by the cells of the immune system of most vertebrates in response to challenges by foreign agents such as viruses, parasites and tumor cells. Interferon-beta (IFN beta) is an extra-cellular protein mediator of host defense and homeostasis. IFN beta has well-established direct antiviral, antiproliferative and immunomodulatory properties. Recombinant IFN beta is approved for the treatment of relapsing-remitting multiple sclerosis. The recombinant IFN beta protein has the theoretical potential to either treat or cause autoimmune neuromuscular disorders by altering the complicated and delicate balances within the immune system networks. It is the most widely prescribed disease-modifying therapy for multiple sclerosis (MS). Large-scale clinical trials have established the clinical efficacy of IFN beta in reducing relapses and slowing disease progression in relapsing-remitting MS. IFN beta therapy was shown to be comparably beneficial for opticospinal MS (OSMS) and conventional MS in Japanese. IFN beta is effective in reducing relapses in secondary progressive MS and may have a modest effect in slowing disability progression. In addition to the common antiviral activity, IFN beta also induces increased production of the p53 gene product which promotes apoptosis, and thus has therapeutic effect against certain cancers. The role of IFN-beta in bone metabolism could warrant its systematic evaluation as a potential adjunct to therapeutic regimens of osteolytic diseases. Furthermore, IFN beta might play a beneficial role in the development of a chronic progressive CNS inflammation.