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Mouse Anti-IL36RN Recombinant Antibody (A564) (CBMAB-AP10883LY)

The product is antibody recognizes IL36RN. The antibody A564 immunoassay techniques such as: ELISA, WB.
See all IL36RN antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
A564
Antibody Isotype
IgG2b
Application
ELISA, WB

Basic Information

Immunogen
Fusion protein of IL1F5
Specificity
Human
Antibody Isotype
IgG2b
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.

Target

Full Name
Interleukin 36 Receptor Antagonist
Introduction
The protein encoded by this gene is a member of the interleukin 1 cytokine family. This cytokine was shown to specifically inhibit the activation of NF-kappaB induced by interleukin 1 family, member 6 (IL1F6). This gene and eight other interleukin 1 family genes form a cytokine gene cluster on chromosome 2. Two alternatively spliced transcript variants encoding the same protein have been reported. [provided by RefSeq, Jul 2008]
Entrez Gene ID
26525
UniProt ID
Q9UBH0
Alternative Names
Interleukin 36 Receptor Antagonist
Function
Inhibits the activity of interleukin-36 (IL36A,IL36B and IL36G) by binding to receptor IL1RL2 and preventing its association with the coreceptor IL1RAP for signaling. Part of the IL-36 signaling system that is thought to be present in epithelial barriers and to take part in local inflammatory response; similar to the IL-1 system with which it shares the coreceptor. Proposed to play a role in skin inflammation. May be involved in the innate immune response to fungal pathogens, such as Aspergillus fumigatus. May activate an anti-inflammatory signaling pathway by recruiting SIGIRR.
Biological Process
Antifungal humoral responseManual Assertion Based On ExperimentIMP:UniProtKB
Cellular response to lipopolysaccharideManual Assertion Based On ExperimentIBA:GO_Central
Inflammatory responseManual Assertion Based On ExperimentIBA:GO_Central
Inflammatory response to antigenic stimulusManual Assertion Based On ExperimentIBA:GO_Central
Innate immune responseIEA:UniProtKB-KW
Negative regulation of cytokine-mediated signaling pathwayManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of interferon-gamma productionManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of interleukin-17 productionManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of interleukin-6 productionIEA:Ensembl
Cellular Location
Cytoplasm; Secreted. The secretion is dependent on protein unfolding and facilitated by the cargo receptor TMED10; it results in protein translocation from the cytoplasm into the ERGIC (endoplasmic reticulum-Golgi intermediate compartment) followed by vesicle entry and secretion.
Involvement in disease
Psoriasis 14, pustular (PSORS14):
A life-threatening disease defined by repeated flares of sudden onset consisting of diffuse erythematous skin eruption characterized by rapid coverage with pustules, high-grade fever, asthenia, marked leukocytosis, and elevated serum levels of C-reactive protein.

Choon, S. E., Tok, P. S. K., Wong, K. W., Lim, Y. T., Nanu, N. M., Barker, J. N., & Capon, F. (2023). Clinical profile of patients with acute generalized pustular psoriasis with and without IL36RN mutations in multi‐ethnic Johor Bahru, Malaysia. Experimental Dermatology.

Tachibana, K., Kawakami, Y., Tokuda, M., Sato, S., Sugihara, S., Miyake, T., ... & Morizane, S. (2022). Flare‐up of generalized pustular psoriasis following Pfizer‐BioNTech BNT162b2 mRNA COVID‐19 vaccine: Two cases without mutations of IL36RN and CARD14 genes. The Journal of Dermatology.

Yoshikawa, M., Rokunohe, D., Kimura, A., Takahashi, M., Korekawa, A., Nakajima, K., ... & Sawamura, D. (2021). Significance of IL36RN mutation analyses in the management of impetigo herpetiformis: A case report and review of published cases. The Journal of Dermatology, 48(5), 699-702.

Liang, J., Zhang, H., Guo, Y., Yang, K., Ni, C., Yu, H., ... & Yao, Z. (2019). Coinheritance of generalized pustular psoriasis and familial Behçet‐like autoinflammatory syndrome with variants in IL 36 RN and TNFAIP 3 in the heterozygous state. The Journal of Dermatology, 46(10), 907-910.

Komatsuda, S., Kamata, M., Chijiwa, C., Namiki, K., Fukaya, S., Hayashi, K., ... & Tada, Y. (2019). Gastrointestinal bleeding with severe mucosal involvement in a patient with generalized pustular psoriasis without IL 36 RN mutation. The Journal of Dermatology, 46(1), 73-75.

Zea-Vera, A. F., Estupiñan-Lopez, F. E., Cifuentes-Burbano, J., Vargas, M. J., & Bonelo, A. (2019). Interleukin-36 receptor antagonist deficiency (DITRA) with a novel IL36RN homozygous mutation c. 200G> T (P. Cys67Phe) in a young Colombian woman. Journal of clinical immunology, 39, 261-263.

Bal, E., Lim, A. C., Shen, M., Douangpanya, J., Madrange, M., Gazah, R., ... & Smahi, A. (2019). Mutation in IL 36 RN impairs the processing and regulatory function of the interleukin‐36‐receptor antagonist and is associated with DITRA syndrome. Experimental Dermatology, 28(10), 1114-1117.

Wilsmann‐Theis, D., Schnell, L. M., Ralser‐Isselstein, V., Bieber, T., Schön, M. P., Hüffmeier, U., & Mössner, R. (2018). Successful treatment with interleukin‐17A antagonists of generalized pustular psoriasis in patients without IL36RN mutations. The Journal of dermatology, 45(7), 850-854.

Zhu, T., Jin, H., Shu, D., Li, F., & Wu, C. (2018). Association of IL36RN mutations with clinical features, therapeutic response to acitretin, and frequency of recurrence in patients with generalized pustular psoriasis. European Journal of Dermatology, 28, 217-224.

Li, Z., Yang, Q., & Wang, S. (2018). Genetic polymorphism of IL36RN in Han patients with generalized pustular psoriasis in Sichuan region of China: A case–control study. Medicine, 97(31).

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

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