IL-9 Protein (AA 19-144) (Fc Tag)
Quick Overview for IL-9 Protein (AA 19-144) (Fc Tag) (ABIN7490679)
Target
See all IL-9 (IL9) ProteinsProtein Type
Origin
Source
Purity
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Protein Characteristics
- AA 19-144
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Purification tag / Conjugate
- This IL-9 protein is labelled with Fc Tag.
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Purpose
- Recombinant Cynomolgus IL9 protein with C-terminal human Fc tag
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Specificity
- IL9 (Arg19-Ile144) hFc (Glu99-Ala330)
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Characteristics
- Extracellular Domain Protein
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Purification
- Purified from cell culture supernatant by affinity chromatography
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Restrictions
- For Research Use only
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Format
- Lyophilized
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Buffer
- Lyophilized from sterile PBS, pH 7.4. Normally 5 % - 8 % trehalose is added as protectants before lyophilization.
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Storage
- -20 °C,-80 °C
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Storage Comment
- Store at -20°C to -80°C for 12 months in lyophilized form. After reconstitution, if not intended for use within a month, aliquot and store at -80°C (Avoid repeated freezing and thawing). Lyophilized proteins are shipped at ambient temperature.
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Expiry Date
- 12 months
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- IL-9 (IL9) (Interleukin 9 (IL9))
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Alternative Name
- IL9
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Background
- Interleukin 9, also known as IL-9, is a cytokine (cell signaling 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 the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-β1 to differentiate naive 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 the 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 the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.
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Molecular Weight
- predicted molecular mass of 40.0 kDa after removal of the signal peptide.
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UniProt
- A0A7N9IA33
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Pathways
- JAK-STAT Signaling
Target
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