Mouse Anti-IL17F Recombinant Antibody (A482) (CBMAB-AP10836LY)

Name: Mouse Anti-IL17F Recombinant Antibody (A482)
SKU: CBMAB-AP10836LY
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

A482

Application

ELISA, WB

Immunogen

Fusion protein of IL-17F

Specificity

Human, Mouse

Antibody Isotype

IgG1

Clonality

Monoclonal

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Purity

Affinity purity

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

More Infomation

Target

Full Name

Interleukin 17F

Introduction

The protein encoded by this gene is a cytokine that shares sequence similarity with IL17. This cytokine is expressed by activated T cells, and has been shown to stimulate the production of several other cytokines, including IL6, IL8, and CSF2/GM_CSF. This cytokine is also found to inhibit the angiogenesis of endothelial cells and induce endothelial cells to produce IL2, TGFB1/TGFB, and monocyte chemoattractant protein-1. [provided by RefSeq, Jul 2008]

Entrez Gene ID

Human	112744
Mouse	257630

UniProt ID

Human	Q96PD4
Mouse	Q7TNI7

Alternative Names

Interleukin 17F

Function

E-AB-27574

Biological Process

Adaptive immune response Source: UniProtKB-KW
Cartilage development Source: UniProtKB
Defense response to Gram-negative bacterium Source: Ensembl
Defense response to Gram-positive bacterium Source: Ensembl
Inflammatory response Source: UniProtKB-KW
Innate immune response Source: UniProtKB-KW
Interleukin-17-mediated signaling pathway Source: UniProtKB
Negative regulation of angiogenesis Source: UniProtKB
Positive regulation of antimicrobial peptide production Source: Ensembl
Positive regulation of chemokine (C-X-C motif) ligand 1 production Source: UniProtKB
Positive regulation of cytokine production Source: UniProtKB
Positive regulation of cytokine production involved in inflammatory response Source: Ensembl
Positive regulation of interleukin-6 production Source: UniProtKB
Positive regulation of lymphotoxin A production Source: UniProtKB
Positive regulation of transcription by RNA polymerase II Source: Ensembl
Regulation of granulocyte macrophage colony-stimulating factor production Source: UniProtKB
Regulation of interleukin-2 production Source: UniProtKB
Regulation of interleukin-6 production Source: UniProtKB
Regulation of interleukin-8 production Source: UniProtKB
Regulation of transforming growth factor beta receptor signaling pathway Source: UniProtKB

Cellular Location

Secreted

Involvement in disease

Candidiasis, familial, 6 (CANDF6):
A primary immunodeficiency disorder with altered immune responses and impaired clearance of fungal infections, selective against Candida. It is characterized by persistent and/or recurrent infections of the skin, nails and mucous membranes caused by organisms of the genus Candida, mainly Candida albicans.

Tam, H. K. J., Robinson, P. C., & Nash, P. (2022). Inhibiting IL-17A and IL-17F in rheumatic disease: Therapeutics help to elucidate disease mechanisms. Current Rheumatology Reports, 24(10), 310-320.

Braga, M., Lara-Armi, F. F., Neves, J. S. F., Rocha-Loures, M. A., Terron-Monich, M. D. S., Bahls-Pinto, L. D., ... & Visentainer, J. E. L. (2021). Influence of IL10 (rs1800896) polymorphism and TNF-α, IL-10, IL-17A, and IL-17F serum levels in ankylosing spondylitis. Frontiers in immunology, 12, 653611.

Iznardo, H., & Puig, L. (2021). Dual inhibition of IL-17A and IL-17F in psoriatic disease. Therapeutic Advances in Chronic Disease, 12, 20406223211037846.

Adams, R., Maroof, A., Baker, T., Lawson, A. D., Oliver, R., Paveley, R., ... & Griffiths, M. (2020). Bimekizumab, a novel humanized IgG1 antibody that neutralizes both IL-17A and IL-17F. Frontiers in Immunology, 11, 1894.

Goepfert, A., Lehmann, S., Blank, J., Kolbinger, F., & Rondeau, J. M. (2020). Structural analysis reveals that the cytokine IL-17F forms a homodimeric complex with receptor IL-17RC to drive IL-17RA-independent signaling. Immunity, 52(3), 499-512.

Gao, S., Mao, C., Cheng, J., Deng, Q., & Sheng, W. (2020). Association of IL‐17A‐197G/A and IL‐17F‐7488T/C polymorphisms and osteoarthritis susceptibility: A meta‐analysis. International Journal of Rheumatic Diseases, 23(1), 37-46.

Burns, L. A., Maroof, A., Marshall, D., Steel, K. J., Lalnunhlimi, S., Cole, S., ... & Taams, L. S. (2020). Presence, function, and regulation of IL‐17F‐expressing human CD4+ T cells. European Journal of Immunology, 50(4), 568-580.

Chen, Y., Chen, Y., Cao, P., Su, W., Zhan, N., & Dong, W. (2020). Fusobacterium nucleatum facilitates ulcerative colitis through activating IL‐17F signaling to NF‐κB via the upregulation of CARD3 expression. The Journal of pathology, 250(2), 170-182.

Glatt, S., Baeten, D., Baker, T., Griffiths, M., Ionescu, L., Lawson, A. D., ... & Shaw, S. (2018). Dual IL-17A and IL-17F neutralisation by bimekizumab in psoriatic arthritis: evidence from preclinical experiments and a randomised placebo-controlled clinical trial that IL-17F contributes to human chronic tissue inflammation. Annals of the rheumatic diseases, 77(4), 523-532.

Tang, C., Kakuta, S., Shimizu, K., Kadoki, M., Kamiya, T., Shimazu, T., ... & Iwakura, Y. (2018). Suppression of IL-17F, but not of IL-17A, provides protection against colitis by inducing Treg cells through modification of the intestinal microbiota. Nature Immunology, 19(7), 755-765.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

Antibody Pairs

IL17F Matched Antibody Pair (619) (CAT#: APMAB-619LY)

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Isotype control

For research use only. Not intended for any clinical use.

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