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 >  Protein>IL-22 >IL2-H8247

Biotinylated Human IL-22 Protein, His,Avitag™

分子别名(Synonym)

IL-22,IL-TIF,ZCYTO18

表达区间及表达系统(Source)

Biotinylated Human IL-22, His,Avitag (IL2-H8247) is expressed from human 293 cells (HEK293). It contains AA Ala 34 - Ile 179 (Accession # Q9GZX6-1).

Predicted N-terminus: His

Request for sequence

蛋白结构(Molecular Characterization)

IL-22 Structure

This protein carries a polyhistidine tag at the N-terminus, followed by an Avi tag (Avitag™)

The protein has a calculated MW of 20.3 kDa. The protein migrates as 25-35 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

标记(Labeling)

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

蛋白标记度(Protein Ratio)

Passed as determined by the HABA assay / binding ELISA.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>90% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

IL-22 SDS-PAGE

Biotinylated Human IL-22, His,Avitag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 90%.

 

活性(Bioactivity)-ELISA

IL-22 ELISA

Immobilized Biotinylated Human IL-22, His,Avitag (Cat. No. IL2-H8247) at 1 μg/mL (100 μL/well)on streptavidin (Cat. No. STN-N5116) precoated (0.5 μg/well) plate. can bind Human IL-22 Antibody with a linear range of 0.1-4 ng/mL (QC tested).

Protocol

IL-22 ELISA

Immobilized Human IL-22 Antibody at 1 μg/mL (100 μL/well) can bind Biotinylated Human IL-22, His,Avitag (Cat. No. IL2-H8247) with a linear range of 1-31 ng/mL (Routinely tested).

Protocol

IL-22 ELISA

Immobilized Biotinylated Human IL-22, His,Avitag (Cat. No. IL2-H8247) at 1 μg/mL (100 μL/well) on streptavidin (Cat. No. STN-N5116) precoated (0.5 μg/well) plate can bind Human IL-22 R alpha 1, Fc Tag (Cat. No. IL1-H5258) with a linear range of 0.6-78 ng/mL (Routinely tested).

Protocol

IL-22 ELISA

Immobilized Human IL-22BP Protein, Fc Tag (Cat. No. ILP-H5254) at 5 μg/mL (100 μL/well) can bind Biotinylated Human IL-22, His,Avitag (Cat. No. IL2-H8247) with a linear range of 0.03-1 ng/mL (Routinely tested).

Protocol

 
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背景(Background)

Interleukin-22 (IL22) is also known as cytokine Zcyto18, IL-10-related T-cell-derived-inducible factor (IL-TIF), which is belongs to the IL-10 family or IL-10 superfamily (including IL-19, IL-20, IL-24, and IL-26), a class of potent mediators of cellular inflammatory responses. IL-22 is produced by activated DC and T cells and initiates innate immune responses against bacterial pathogens especially in epithelial cells such as respiratory and gut epithelial cells. IL-22 biological activity is initiated by binding to a cell-surface complex composed of IL-22R1 and IL-10R2 receptor chains and further regulated by interactions with a soluble binding protein IL-22BP. IL-22 also promotes hepatocyte survival in the liver and epithelial cells in the lung and gut similar to IL-10.

 

前沿进展

The metabolic sensor LKB1 regulates ILC3 homeostasis and mitochondrial function
Fonseca-Pereira, Bae, Clay et al
Cell Rep (2025) 44 (4), 115456
Abstract: Group 3 innate lymphoid cells (ILC3s) are tissue-resident cells that sense environmental cues, control infections, and promote tissue homeostasis at mucosal surfaces. The metabolic sensor liver kinase B1 (LKB1) integrates intracellular stress, metabolism, and mitochondrial function to promote the development and effector functions of a variety of immune cells; however, the role of LKB1 in ILC3 function was unknown. Here, we show that LKB1 is crucial for adult ILC3 homeostasis, cytokine production, and mitochondrial function. ILC3-specific LKB1 deletion resulted in a reduced number of ILC3s and interleukin-22 (IL-22) production. LKB1-deficient ILC3s had decreased survival, mitochondrial dysfunction, cytoplasmic lipid accumulation, and altered bioenergetics. Using LKB1 downstream kinase modulators, we found that LKB1 regulation of ILC3 survival and IL-22 production requires signaling through microtubule affinity-regulating kinases (MARKs). Mechanistically, LKB1 deficiency resulted in increased reactive oxygen species (ROS) production and NFAT2 and PD-1 expression. Our work reveals that metabolic regulation of enteric ILC3 function by an LKB1-dependent signaling network is crucial for intestinal immunity and tissue homeostasis.Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.
NLRP3 inflammasome-based therapies by natural products: a new development in the context of cancer therapy
Owida, Abed, Altalbawy et al
Naunyn Schmiedebergs Arch Pharmacol (2025)
Abstract: The leucine-rich repeat containing protein (NLR) canonical inflammasome family includes Nod-like receptor protein 3 (NLRP3). Via the mediation of apoptosis proteins and immunological reactions, it controls the pathogenesis of malignancy. Experimental studies showed a relationship among lymphogenesis, cancer metastasis, and NLRP3 expression. Natural products have also been used as lead-based substances in a number of investigations to speed up the creation of novel, specific NLRP3 inhibitors. Via the mediation of apoptotic proteins and immunological responses, it controls the pathogenesis of malignancy. Moreover, it was recently noted that among human cancers, chemotherapy activates NLRP3. Induction of NLRP3 could encourage the generation of IL-1β and IL-22 to facilitate the propagation of malignancy. Additionally, prior research has demonstrated that the usage of NLRP3 in cancer therapy may result in resistance to drugs. The depletion of NLRP3 could affect the survival of cells. Natural products have been used as lead materials in a number of studies to help generate novel, specific NLRP3 antagonists more quickly. In the present review, we examine the mechanism behind the beneficial effects of the natural substances on the inhibition of cancer growth and progression, with special focus on NLRP3 regulation.© 2025. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
Fluxapyroxad induces chronic colonic inflammation via inhibiting intestinal aryl hydrocarbon receptors in mice
Cao, Xiao, Fang et al
Sci Total Environ (2025) 973, 179134
Abstract: Fluxapyroxad, the most extensively utilized succinate dehydrogenase inhibitor (SDHI) fungicide, lacks comprehensive research on potential risks associated with chronic toxicity. To investigate its effects on chronic colonic inflammation and elucidate the underlying mechanisms, a mouse model was employed to assess oral exposure to fluxapyroxad at no observed adverse effect level (NOEL) for 13 weeks, in vitro and in silico models were utilized as well. The results revealed reduced body weight gain, colon length reduction, crypt damage, goblet cell loss in the colon, impaired intestinal barrier integrity, and an elevation of proinflammatory cytokines, including IL-6, IL-1β, and TNF-α following fluxapyroxad exposure in mice. These findings suggested that fluxapyroxad induced chronic colonic inflammation. Furthermore, fluxapyroxad decreased interleukin 22 levels and antibacterial peptide secretion by inhibiting Aryl hydrocarbon receptors (AhR) activation, which was confirmed in vitro experiments. Molecular docking analysis indicated that fluxapyroxad spontaneously formed halogen bonds and bound hydrophobic interactions with AhR, which might act as an AhR inhibitor. These results indicated that AhR inhibition may represent one of the primary mechanisms for chronic colonic inflammation induced by fluxapyroxad exposure. This study shed light on the association between low acute pesticide exposure to fluxapyroxad and chronic colonic inflammation development while contributing to pesticide safety assessment.Copyright © 2025. Published by Elsevier B.V.
Polymorphisms in IL-10- and IL-22-Binding Protein Genes as Genetic Predictors of the Direct-Acting Antivirals Treatment Response in Patients with Chronic Hepatitis C Virus
Saleem, Akbar, Jilkova et al
J Interferon Cytokine Res (2025)
Abstract: Cytokines are crucial in controlling inflammation during viral infection, particularly infection with the hepatitis C virus (HCV). Cytokine genetic polymorphisms can change how the immune system responds to this infection. We investigated how the HCV infection treatment was affected by single nucleotide polymorphisms in these genes. The goal of this study was to examine any connections between the cytokine gene polymorphisms for interleukins (IL)-22-binding protein rs6570136, as well as IL-10 rs1800872 and rs1878672 in the Pakistani population and responsiveness to direct-acting antivirals (DAAs) treatment. This study evaluated 155 participants, which included 55 patients who achieved sustained virologic response (SVR), 40 relapse patients, and 60 healthy controls, to assess and compare the clinical parameters. The SVR and relapse groups were compared for their allelic and genotypic frequencies. We discovered that the SVR and the relapse groups had significantly different genotype frequencies for IL-10 rs1800872 and IL-22BP rs6570136 in the Pakistani population. The G/G genotype in rs6570136 and A/A genotype in rs1800872 were significantly associated with relapse following DAA therapy, with P values 0.002 and 0.0004, respectively. In contrast, rs1878672 showed no significant correlation with HCV relapse, P = 0.63.
Showing 1-4 of 5861 papers.
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IL-22靶点信息
英文全称:Interleukin-22
中文全称:白细胞介素-22
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:3详情
最高研发阶段:临床三期
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