Recombinant Mouse IL-17A Protein (C-6His)

Beta LifeScience SKU/CAT #: BL-2121NP
BL-2121NP: Greater than 95% as determined by reducing SDS-PAGE. (QC verified)
BL-2121NP: Greater than 95% as determined by reducing SDS-PAGE. (QC verified)

Recombinant Mouse IL-17A Protein (C-6His)

Beta LifeScience SKU/CAT #: BL-2121NP
Our products are highly customizable to meet your specific needs. You can choose options such as endotoxin removal, liquid or lyophilized forms, preferred tags, and the desired functional sequence range for proteins. Submitting a written inquiry expedites the quoting process.

Submit an inquiry today to inquire about all available size options and prices! Connect with us via the live chat in the bottom corner to receive immediate assistance.

Product Overview

Description Recombinant Mouse Interleukin-17A is produced by our Mammalian expression system and the target gene encoding Thr22-Ala158 is expressed with a 6His tag at the C-terminus.
Accession Q62386
Synonym Interleukin-17A; IL-17; IL-17A; Cytotoxic T-Lymphocyte-Associated Antigen 8; CTLA-8; IL17A; CTLA8; IL17
Gene Background Interleukin-17 is a potent pro-inflammatory cytokine produced by activated memory T cells. There are at least six members of the IL-17 family in humans and in mice. Mature mouse IL-17A shares 61% and 89% amino acid sequence identity with human and rat IL-17A, respectively. As IL-17 shares properties with IL-1 and TNF-alpha, it may induce joint inflammation and bone and cartilage destruction. This cytokine is found in synovial fluids of patients with rheumatoid arthritis, and produced by rheumatoid arthritis synovium. It increases IL-6 production, induces collagen degradation and decreases collagen synthesis by synovium and cartilage and proteoglycan synthesis in cartilage. IL-17 is also able to increase bone destruction and reduce its formation. Blocking of interleukin-17 with specific inhibitors provides a protective inhibition of cartilage and bone degradation.
Molecular Mass 16.2 KDa
Apmol Mass 17-26 KDa, reducing conditions
Formulation Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.
Endotoxin Less than 0.001 ng/µg (0.01 EU/µg) as determined by LAL test.
Purity Greater than 95% as determined by reducing SDS-PAGE. (QC verified)
Biological Activity Biologically active. Please contact us to obtain bioactivity data.
Reconstitution Always centrifuge tubes before opening. Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles.
Storage Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months.
Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature listed below.
Usage For Research Use Only

Target Details

Target Function Effector cytokine of innate and adaptive immune system involved in antimicrobial host defense and maintenance of tissue integrity. Signals via IL17RA-IL17RC heterodimeric receptor complex, triggering homotypic interaction of IL17RA and IL17RC chains with TRAF3IP2 adapter. This leads to downstream TRAF6-mediated activation of NF-kappa-B and MAPkinase pathways ultimately resulting in transcriptional activation of cytokines, chemokines, antimicrobial peptides and matrix metalloproteinases, with potential strong immune inflammation. Plays an important role in connecting T cell-mediated adaptive immunity and acute inflammatory response to destroy extracellular bacteria and fungi. As a signature effector cytokine of T-helper 17 cells (Th17), primarily induces neutrophil activation and recruitment at infection and inflammatory sites. In airway epithelium, mediates neutrophil chemotaxis via induction of CXCL1 and CXCL5 chemokines. In secondary lymphoid organs, contributes to germinal center formation by regulating the chemotactic response of B cells to CXCL12 and CXCL13, enhancing retention of B cells within the germinal centers, B cell somatic hypermutation rate and selection toward plasma cells. Effector cytokine of a subset of gamma-delta T cells that functions as part of an inflammatory circuit downstream IL1B, TLR2 and IL23A-IL12B to promote neutrophil recruitment for efficient bacterial clearance. Effector cytokine of innate immune cells including invariant natural killer cell (iNKT) and group 3 innate lymphoid cells that mediate initial neutrophilic inflammation. Involved in the maintenance of the integrity of epithelial barriers during homeostasis and pathogen infection. Upon acute injury, has a direct role in epithelial barrier formation by regulating OCLN localization and tight junction biogenesis. As part of the mucosal immune response induced by commensal bacteria, enhances host's ability to resist pathogenic bacterial and fungal infections by promoting neutrophil recruitment and antimicrobial peptides release. In synergy with IL17F, mediates the production of antimicrobial beta-defensins DEFB1, DEFB103A, and DEFB104A by mucosal epithelial cells, limiting the entry of microbes through the epithelial barriers. Involved in antiviral host defense through various mechanisms. Enhances immunity against West Nile virus by promoting T cell cytotoxicity. May play a beneficial role in influenza A virus (H5N1) infection by enhancing B cell recruitment and immune response in the lung. Contributes to influenza A virus (H1N1) clearance by driving the differentiation of B-1a B cells, providing for production of virus-specific IgM antibodies at first line of host defense.
Subcellular Location Secreted.
Protein Families IL-17 family
Database References
Tissue Specificity Expressed by Th17 cell lineage (at protein level). The expression pattern reflects the differentiation state, with IL17A-IL17F heterodimers produced at higher levels than IL17A-IL17A and IL17F-IL17F dimers in fully differentiated Th17 cells. Expressed in

Gene Functions References

  1. gammadeltaT17 cells constitutively express chemokine receptors CCR6 and CCR2 PMID: 28580944
  2. this paper shows that IL-17-driven intestinal fibrosis is inhibited by Itch-mediated ubiquitination of HIC-5 PMID: 28612841
  3. this study shows that IL-17A negatively regulates lymphangiogenesis in T helper 17 cell-mediated inflammation PMID: 28930285
  4. The present study demonstrated that a high fat diet induces IL-17A expression, which exacerbates the progression of nonalcoholic fatty liver disease by inhibiting fatty acid beta-oxidation and promoting the accumulation of triglycerides (TG). PMID: 28153707
  5. JunB has an essential role in IL-23-dependent pathogenicity of Th17 cells PMID: 28555647
  6. Gamma-delta T cells are a prime source of protumoral IL17A in breast cancer. PMID: 29070614
  7. blocking activin/ACVR2A impaired the potency of hepatic stellate cells to produce collagens in response to IL17s. PMID: 29620144
  8. this study shows the positive effects of IL-17 on the early-stage differentiation and negative effects on the calcification of primary osteoblasts in vitro PMID: 29438885
  9. these data suggest that IL-17A promotes DVT pathogenesis by enhancing platelet activation and aggregation, neutrophil infiltration, and EC activation PMID: 29482157
  10. These findings highlight a regulatory pathway of Tiam1/Rac1 in Th17 cells and suggest that it may be a therapeutic target in multiple sclerosis. PMID: 27725632
  11. DAPK deficiency leads to excess HIF-1a accumulation, enhanced IL-17 expression and exacerbated experimental autoimmune encephalomyelitis. PMID: 27312851
  12. decreased COX-2 and IL-17 levels were observed in both groups treated with Nintedanib in the prostate anterior lobe. Thus, we concluded that Nintedanib was effective in delaying tumor progression and, despite not directly acting on inflammation, Nintedanib may adversely affect inflammatory pathways, favoring prostate cancer delay PMID: 29429524
  13. In studies of mouse and human pancreatic tumors and precursors, we found that immune cell-derived IL17 regulated development of tuft cells and stem cell features of pancreatic cancer cells via increased expression of DCLK1, POU2F3, ALDH1A1, and IL17RC. PMID: 29604293
  14. The reaction of IL-17A in the acute lung injury induced by LPS is stronger than that by PQ. PMID: 28600744
  15. IL17A promoted osteoblast differentiation and calcification in a partly AKT2dependent manner in MC3T3E1 cells in vitro, possibly reflecting compensation by other signaling pathways. The results of the present study may offer novel perspectives to guide the clinical strategy for the prevention and treatment of periodontitis PMID: 28849233
  16. Mechanistically, CREB, activated by CD3-PKC- signaling, plays a key role in regulating Th17 cell differentiation, at least in part through directly binding to the Il17-Il17f gene locus. PMID: 29050947
  17. Data show that interleukin-17 (IL-17) and fungal candidalysin amplify inflammation in a self-reinforcing feed-forward loop. PMID: 29101209
  18. The data indicate that IL-17A contributes to augmented responses to ozone in db/db mice. Furthermore, IL-17A appears to act at least in part by inducing expression of gastrin-releasing peptide receptor. PMID: 28957638
  19. miR203 expression may be upregulated by IL17 stimulation, and miR203 is a positive regulator of IL17induced VEGF secretion. PMID: 29039484
  20. IL-17 contributes to lung obliterative bronchiolitis pathogenesis through regulating macrophages function PMID: 28863322
  21. we demonstrate that gammadelta T cells and CD4+ T (Th17) cells are the two major producers of IL-17A in the lung at the early and later stages of chlamydial infection, respectively PMID: 27796286
  22. In mice on a C57BL/6 background, neither IL-23p19 nor IL-17A plays a role for immune protection against L. major in the physiological context of natural infections. PMID: 27297018
  23. IL-17A and IL-17F exert distinct biological effects during pulmonary infection; the IL-17F/IL-17RC signaling axis has the potential to significantly worsen pathogen-associated inflammation of the lower respiratory tract. PMID: 28813677
  24. TLR2/4-mediated IL-17A inflammatory signaling is involved in vessel degeneration and revascularization, indicating that modulation of the TLR2/4-IL-17A pathway may be a novel therapeutic strategy for degenerative diseases. PMID: 27297042
  25. The hormone levels are significantly reduced and lymphocytic infiltration in the lacrimal gland in ovariectomized mice, whereas the frequency of Th17 cells in the blood and spleen and IL-17A and IL-23 expression in the lacrimal glands are increased, leading to reduced tear production and positive fluorescein staining in the cornea. PMID: 27341090
  26. the results suggest that IL-17A induces podocyte injury by activating the NLRP3 inflammasome and IL-1beta secretion and contributes to disruption of the kidney's filtration system. PMID: 29446486
  27. These results suggest that a low concentration of IL-17A is likely to promote autophagic activity via activating RANKL-JNK pathway during osteoclastogenesis. PMID: 29476739
  28. study shows that IL-17A plays an important role in comorbid depression associated with psoriatic inflammation, where both NFkappaB and p38MAPK pathways play significant roles via upregulation of inflammatory mediators in the brain PMID: 28570931
  29. the present study demonstrated that IL-17A crucially regulated the wound healing process and that accelerated neutrophil accumulation caused by IL-17A led to the delayed wound repair. PMID: 27305096
  30. The results emphasize the importance of IL-17 in experimental autoimmune myasthenia gravis development and that IL-17 independent pathways drive the autoimmune reaction. PMID: 28599246
  31. In estrogen receptor negative breast cancer cells targeting of IL-17A inhibited PDL1 expression in the tumor microenvironment, decreasing the percentage of Treg cells in tumor-infiltrating lymphocytes, and promoting CD4+ and CD8+ T cells to secrete interferon gamma. PMID: 27935862
  32. Report provides evidence that IL-17 can promote Lewis lung carcinoma growth through inhibition of myeloid-derived suppressor cells apoptosis, which maybe dependent on ERK1/2 signaling pathway. PMID: 28002798
  33. these data provide novel insight into a dynamic IL-17A-CXCR2-neutrophil axis during acute segmented filamentous bacteria colonization and demonstrate a central role for neutrophils in limiting segmented filamentous bacteria expansion PMID: 27624780
  34. Transient AIEC colonization in IL-17 KO mice resulted in increased intestinal epithelial damage, systemic bacterial burden and mortality compared with controls. IL-17 is required for the induction of IL-22 during AIEC strain E. coli LF82 colonization. IL-17 plays a protective role in AIEC strain E. coli LF82 induced colitis by promoting IL-22 secretion. PMID: 29195141
  35. after orthotopic lung transplantation, in the IL-17A KO group, less inflammation in the bronchovascular axis was observed and a non-significant trend towards less bronchovascular fibrosis, pleural/septal inflammation and fibrosis, and parenchymal inflammation and fibrosis when compared to WT mice PMID: 27737799
  36. Data show that IL-17 in the serum of collagen-induced arthritis (CIA) mice was markedly increased on day 14 and reached its apogee on day 27. PMID: 27356747
  37. this study unveiled the role of IL-23-dependent IL-17 induction in LdCen-/- parasite-induced immunity and subsequent protection against visceral leishmaniasis PMID: 29187586
  38. There was a significantly decreased percentage of IL-17A-producing CD4 T cells in mice receiving Tregs from xIAP mice. xIAP appears dispensable for the generation of induced Treg cells as well as function of natural Treg cells. There appeared to be a role of xIAP in generation of IL-17-producing cells from either naive CD4 T cells or Treg cells. PMID: 26825770
  39. astrocytic IL-17A plays important roles in the maintenance of neuropathic pain through CaMKII/CREB signaling pathway in spinal cord. PMID: 26166359
  40. Results reveal the importance of the IL-23/IL-17 inflammatory axis in secondary brain injury after intracerebral hemorrhage. PMID: 27729335
  41. these results demonstrate an important role of CXCR6 in the regulation of pathological Th17 and IL-17A(+)TCRgammadelta(+) T-cell recruitment into atherosclerotic lesions. PMID: 26614640
  42. These results suggest that IL-17A plays an important role in host survival against Toxoplasma gondii infection by protecting the host from an anaphylactic reaction via the downregulation of Toxoplasma gondii HSP70 and IFN-gamma production. PMID: 28893913
  43. These results suggest that AKI after septic shock is driven through IL-17 release by Th17 cells; this is gradually consumed in the kidney. PMID: 27515003
  44. IL-17A markedly induced VEGF and IL-6 expression in the Raw264.7 murine macrophage cell line and in the mouse corneal fibroblasts. PMID: 27419340
  45. Vgamma4 T cells accelerate skin graft rejection by providing an early source of IL-17A PMID: 28733202
  46. IL-17 inhibits adipogenesis where a lack of IL-17 ameliorates glucose metabolism. As well, the inhibition of TBK1 reduces inflammation induced by IL-17. Therefore, IL-17 may be involved in the development of obesity and metabolic dysfunction in a TBK1-dependent manner. PMID: 28237848
  47. Th17 cells and TGFbeta1 are not required for the maintenance of gammadelta T cells producing interleukin-17A cells. PMID: 27649780
  48. Data show that inducible T cell co-stimulator (ICOS) deficient mice have a significant increase in the population of IL-17-producing Vgamma2+ gammadelta T cells in the thymus, spleen, lymph nodes and skin and exhibit exacerbated sensitization responses to 2,4-dinitrofluorobenzene. PMID: 27235509
  49. the majority of gammadelta T cells in the non-pregnant uterus, pregnant uterus, decidua and placenta of mice express the transcription factor RORgammat and produce interleukin-17 (IL-17). PMID: 27241697
  50. In both the high-glucose - treated Muller cells and Akita mouse retina, the Act1/TRAF6/IKK/NF-kappaB signaling pathway was activated. IL-17A further enhanced inflammatory signaling activation, whereas Act1 knockdown or IKK inhibition blocked the downstream signaling activation by IL-17A. PMID: 27980343

FAQs

Please fill out the Online Inquiry form located on the product page. Key product information has been pre-populated. You may also email your questions and inquiry requests to sales1@betalifesci.com. We will do our best to get back to you within 4 business hours.

Feel free to use the Chat function to initiate a live chat. Our customer representative can provide you with a quote immediately.

Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

To learn more about how to properly dissolve the lyophilized recombinant protein, please visit Lyophilization FAQs.

Recently viewed