Goat Anti-IL17C (aa160-172) Antibody
Goat Anti-IL17C (aa160-172) Antibody (AF4142a)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
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Primary Accession | Q9P0M4 |
Other Accession | NP_037410.1, 27189 |
Reactivity | Human |
Predicted | Human |
Concentration | 100ug/200ul |
Calculated MW | 21765 Da |
Gene ID | 27189 |
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Other Names | Interleukin-17C, IL-17C, Cytokine CX2, IL17C |
Immunogen | Peptide with sequence RRPCSRDGSGLPT, from the internal region of the protein sequence according to NP_037410.1. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | Goat Anti-IL17C (aa160-172) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | IL17C |
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Function | Cytokine that plays a crucial role in innate immunity of the epithelium, including to intestinal bacterial pathogens, in an autocrine manner. Stimulates the production of antibacterial peptides and pro-inflammatory molecules for host defense by signaling through the NF-kappa-B and MAPK pathways. Acts synergically with IL22 in inducing the expression of antibacterial peptides, including S100A8, S100A9, REG3A and REG3G. Synergy is also observed with TNF and IL1B in inducing DEFB2 from keratinocytes. Depending on the type of insult, may have both protective and pathogenic properties, either by maintaining epithelial homeostasis after an inflammatory challenge or by promoting inflammatory phenotype. Enhanced IL17C/IL17RE signaling may also lead to greater susceptibility to autoimmune diseases. |
Cellular Location | Secreted. |
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Background
Cytokine that plays a crucial role in innate immunity of the epithelium, including to intestinal bacterial pathogens, in an autocrine manner. Stimulates the production of antibacterial peptides and proinflammatory molecules for host defense by signaling through the NF-kappa-B and MAPK pathways. Acts synergically with IL22 in inducing the expression of antibacterial peptides, including S100A8, S100A9, REG3A and REG3G. Synergy is also observed with TNF and IL1B in inducing DEFB2 from keratinocytes. Depending on the type of insult, may have both protective and pathogenic properties, either by maintaining epithelial homeostasis after an inflammatory challenge or by promoting inflammatory phenotype. Enhanced IL17C/IL17RE signaling may also lead to greater susceptibility to autoimmune diseases.
References
Li H.,et al.Proc. Natl. Acad. Sci. U.S.A. 97:773-778(2000).
Zhang W.,et al.Submitted (APR-1999) to the EMBL/GenBank/DDBJ databases.
Clark H.F.,et al.Genome Res. 13:2265-2270(2003).
Song X.,et al.Nat. Immunol. 12:1151-1158(2011).
Ramirez-Carrozzi V.,et al.Nat. Immunol. 12:1159-1166(2011).
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