|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive ,Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A polyhistidine-tag is an amino acid motif in proteins that consists of at least five histidine (His) residues, often at the N- or C-terminus of the protein.
Polyhistidine-tags are often used for affinity purification of polyhistidine-tagged recombinant proteins expressed in Escherichia coli and other prokarfyotic expression systems.
|Mouse IL9 ORF mammalian expression plasmid, C-GFPSpark tag||MG51302-ACG|
|Mouse IL9 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG51302-ACR|
|Mouse IL9 ORF mammalian expression plasmid, C-Flag tag||MG51302-CF|
|Mouse IL9 ORF mammalian expression plasmid, C-His tag||MG51302-CH|
|Mouse IL9 ORF mammalian expression plasmid, C-Myc tag||MG51302-CM|
|Mouse IL9 ORF mammalian expression plasmid, C-HA tag||MG51302-CY|
|Mouse IL9 Gene cDNA clone plasmid||MG51302-G|
|Mouse IL9 ORF mammalian expression plasmid, N-Flag tag||MG51302-NF|
|Mouse IL9 ORF mammalian expression plasmid, N-His tag||MG51302-NH|
|Mouse IL9 ORF mammalian expression plasmid, N-Myc tag||MG51302-NM|
|Mouse IL9 ORF mammalian expression plasmid, N-HA tag||MG51302-NY|
|Mouse IL9 natural ORF mammalian expression plasmid||MG51302-UT|
|Learn more about expression Vectors|
Interleukin 9, also known as IL-9, is a cytokine (cell signalling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells, synergizes with TGF-β1 to differentiate naïve CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight a role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.