Human Interleukin-13 _ IL-13 ProteinVector: CHO
- Known as:
- Human Interleukin-13 _ Interleukin-13 ProteinVector: CHO
- Catalog number:
- 10337-H00C
- Product Quantity:
- 20μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human Interleukin-13 _ IL-13 ProteinVector: CHO
Related genes to: Human Interleukin-13 _ IL-13 ProteinVector: CHO
- Gene:
- IL13 NIH gene
- Name:
- interleukin 13
- Previous symbol:
- -
- Synonyms:
- P600, IL-13, ALRH, BHR1, MGC116786, MGC116788, MGC116789
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-04-07
- Date modifiied:
- 2016-10-05
- Gene:
- IL13RA2 NIH gene
- Name:
- interleukin 13 receptor subunit alpha 2
- Previous symbol:
- -
- Synonyms:
- IL-13R, IL13BP, CD213a2, CT19
- Chromosome:
- Xq23
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-26
- Date modifiied:
- 2015-12-11
Related products to: Human Interleukin-13 _ IL-13 ProteinVector: CHO
Related articles to: Human Interleukin-13 _ IL-13 ProteinVector: CHO
- Progressive IL-13 signaling is closely associated with liver fibrosis. Among fibrotic diseases, liver fibrosis induced by in advanced schistosomiasis is the primary driver of portal hypertension, which is the leading cause of mortality in affected patients. RNA sequencing analysis of human hepatic stellate cells revealed that was markedly upregulated in activated hepatic stellate cells and enriched in the cytokine-receptor interaction pathways, suggesting a potential role for IL-13RA2 in hepatic stellate cell activation and fibrosis progression. Based on these findings, we aimed to investigate whether IL-13RA2 also contributes to liver fibrosis during infection. In this study, we established a murine model of infection. Compared with IL-13RA1, IL-13RA2 expression was significantly increased at week 9 post-infection in mice. IL-13RA2 was enriched within fibrotic regions and increased in parallel with collagen accumulation and stellate cell activation. The phosphorylation levels of MEK and ERK changed in parallel with IL-13RA2 abundance. Furthermore, overexpression of IL-13RA2 markedly accelerated hepatic fibrogenesis, while knockdown of IL-13RA2 attenuated liver fibrosis induced by schistosomiasis the MEK/ERK pathway. Hence, IL-13RA2 may represent an effective and promising therapeutic target for the attenuation of liver fibrosis. - Source: PubMed
Publication date: 2026/04/25
Xiong RuiyanDu JiangyuanYang YuchenZhu YuxiaoNi YangyueChen LinHou MinXu ZhipengChen LuJi Minjun - The clinical manifestations of atopic dermatitis (AD) and chronic nodular prurigo (CNPG) include pruritus and eczema/lesions, posing significant challenges for patients. Th2 cells and ILC2, marked by cytokine production-particularly IL-4/13-are crucial therapeutic targets. Despite displaying a dose-dependent lack of pruritus induction post-injection, IL-13 acts through the IL-13Rα1 and IL-13Rα2 receptor system. Our study focused on investigating ex vivo skin biopsies in AD (n = 17), CNPG (n = 14) and healthy controls (HC; n = 10), examining the gene expression landscape of interleukins linked with pruritus (IL-13, IL-4, IL-31) and their corresponding receptors. Compared to HC, results revealed a significant upregulation of , , and in AD, whereas CNPG did not show increased expression. Notably, the decoy receptor displayed intriguing patterns, with AD showing a marked increase compared to both HC and CNPG. Positive correlations between receptor expression and itch intensity and hyperkinesis sensation underscore clinical relevance, potentially serving as biomarkers. The findings suggest a pivotal role of IL-4 and IL-13, along with IL-13RA1, in pruritus pathogenesis in both entities, while upregulation in AD is countered by IL-13RA2. The comparable expression of to HC in CNPG suggests the absence of this regulatory mechanism, potentially worsening the disease and leading to prolonged scratching behavior. These insights illuminate the intricate interplay of interleukins and receptors in different pruritus phenotypes, laying the groundwork for understanding underlying mechanisms and offering avenues for therapeutic intervention. - Source: PubMed
Publication date: 2024/08/02
Wiegmann HenningRenkhold LinaZeidler ClaudiaAgelopoulos KonstantinStänder Sonja - Our study aimed to explore the association of , and genes polymorphisms with PTB susceptibility and its clinical features. - Source: PubMed
Publication date: 2022/08/08
Li Hong-MiaoTang FeiHuang QianPan Hai-FengZhang Tian-Ping - Atopic asthma and allergic rhinitis are common chronic inflammatory diseases affecting lower airways and nasal mucosa, respectively. Several reports demonstrated frequent co-occurrence of these two diseases, however, the exact molecular mechanism has not been described. The present study aimed to investigate if small non-coding RNA might be responsible for the co-occurrence of asthma and allergic rhinitis in an animal model of allergic airway inflammation. - Source: PubMed
Publication date: 2022/05/07
Langwiński WojciechSzczepankiewicz DawidNarożna BeataStegmayr JohnWagner DarcyAlsafadi HaniLindstedt SandraStachowiak ZuzannaNowakowska JoannaSkrzypski MarekSzczepankiewicz Aleksandra - To identify the role of serum IL-13, and its receptor subunit expressions as a serologic marker of rheumatoid arthritis (RA)-associated ILD (RA-ILD). - Source: PubMed
Publication date: 2021/02/26
Hussein Manal ShawkyEl-Barbary Amal MohamadNada Doaa WaseemGaber Rasha AhmadElkolaly Reham MohamedAboelhawa Marwa Ahmed