Rat Anti-IL36G Recombinant Antibody (CBYY-I0212) (CBMAB-I0562-YY)

Name: Rat Anti-IL36G Recombinant Antibody (CBYY-I0212)
SKU: CBMAB-I0562-YY
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

Rat

Clone

CBYY-I0212

Application

WB, BL

Specificity

Human

Antibody Isotype

IgG2a

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

Lyophilized

Buffer

0.2 μm filtered solution in with Trehalose

Storage

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

More Infomation

Target

Full Name

Interleukin 36 Gamma

Introduction

The protein encoded by this gene is a member of the interleukin 1 cytokine family. The activity of this cytokine is mediated by interleukin 1 receptor-like 2 (IL1RL2/IL1R-rp2), and is specifically inhibited by interleukin 1 family, member 5 (IL1F5/IL-1 delta). Interferon-gamma, tumor necrosis factor-alpha and interleukin 1, beta (IL1B) are reported to stimulate the expression of this cytokine in keratinocytes. The expression of this cytokine in keratinocytes can also be induced by a contact hypersensitivity reaction or herpes simplex virus infection. This gene and eight other interleukin 1 family genes form a cytokine gene cluster on chromosome 2. Two alternatively spliced transcript variants encoding different isoforms have been found for this gene.

Entrez Gene ID

56300

UniProt ID

Q9NZH8

Alternative Names

Interleukin 36 Gamma

Function

Cytokine that binds to and signals through the IL1RL2/IL-36R receptor which in turn activates NF-kappa-B and MAPK signaling pathways in target cells. 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 IL1RAP. Seems to be involved in skin inflammatory response by acting on keratinocytes, dendritic cells and indirectly on T-cells to drive tissue infiltration, cell maturation and cell proliferation. In cultured keratinocytes induces the expression of macrophage, T-cell, and neutrophil chemokines, such as CCL3, CCL4, CCL5, CCL2, CCL17, CCL22, CL20, CCL5, CCL2, CCL17, CCL22, CXCL8, CCL20 and CXCL1; also stimulates its own expression and that of the prototypic cutaneous proinflammatory parameters TNF-alpha, S100A7/psoriasin and inducible NOS. May play a role in proinflammatory responses during particular neutrophilic airway inflammation: activates mitogen-activated protein kinases and NF-kappa B in primary lung fibroblasts, and stimulates the expression of IL-8 and CXCL3 and Th17 chemokine CCL20 in lung fibroblasts. May be involved in the innate immune response to fungal pathogens, such as Aspergillus fumigatus.

Biological Process

Cell-cell signalingManual Assertion Based On ExperimentTAS:ProtInc
Cellular response to lipopolysaccharideManual Assertion Based On ExperimentIBA:GO_Central
Cytokine-mediated signaling pathwayManual 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
Positive regulation of gene expressionManual Assertion Based On ExperimentIBA:GO_Central

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.

PTM

N-terminal truncation leads to a dramatic enhancement of its activity (>1000-fold) (PubMed:21965679).
Proteolytically cleaved by cathepsin CTSG (PubMed:30804664).

Moreira, C. R., de Alcântara, C. C., Flauzino, T., Martin, L. M. M., Lozovoy, M. A. B., Reiche, E. M. V., & Simão, A. N. C. (2023). IL36G genetic variant is independently associated with susceptibility, severity and joint involvement in psoriasis. Molecular Immunology, 159, 69-75.

Merleev, A., Ji-Xu, A., Toussi, A., Tsoi, L. C., Le, S. T., Luxardi, G., ... & Maverakis, E. (2022). Proprotein convertase subtilisin/kexin type 9 is a psoriasis-susceptibility locus that is negatively related to IL36G. JCI insight, 7(16).

Lu, Y. W., Chen, Y. J., Shi, N., Yang, L. H., Wang, H. M., Dong, R. J., ... & Li, Y. Y. (2022). IL36G is associated with cutaneous antiviral competence in psoriasis. Frontiers in Immunology, 13, 971071.

Furue, K., Ito, T., Tanaka, Y., Yumine, A., Hashimoto-Hachiya, A., Takemura, M., ... & Furue, M. (2019). Cyto/chemokine profile of in vitro scratched keratinocyte model: Implications of significant upregulation of CCL20, CXCL8 and IL36G in Koebner phenomenon. Journal of dermatological science, 94(1), 244-251.

Traks, T., Keermann, M., Prans, E., Karelson, M., Loite, U., Kõks, G., ... & Kingo, K. (2019). Polymorphisms in IL36G gene are associated with plaque psoriasis. BMC Medical Genetics, 20, 1-8.

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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)
Proteogenomics
Other Protocols

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Isotype control

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

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