mAb mouse anti-monkey IL-13 Cy5-labeled, clone QS-13
- Known as:
- mAb mouse (anti-) to-monkey Interleukin-13 cynanin 5-labeled, clonality QS-13
- Catalog number:
- ct119
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- U-CyTech biosciences
- Gene target:
- mAb mouse anti-monkey IL-13 Cy5-labeled clone QS-13
Related genes to: mAb mouse anti-monkey IL-13 Cy5-labeled, clone QS-13
- 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: mAb mouse anti-monkey IL-13 Cy5-labeled, clone QS-13
Related articles to: mAb mouse anti-monkey IL-13 Cy5-labeled, clone QS-13
- 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 - The vicious itch-scratch cycle is a cardinal feature of atopic dermatitis (AD), in which IL-13 signaling plays a dominant role. Keratinocytes express two receptors: The heterodimeric IL-4Rα/IL-13Rα1 and IL-13Rα2. The former one transduces a functional IL-13 signal, whereas the latter IL-13Rα2 works as a nonfunctional decoy receptor. To examine whether scratch injury affects the expression of IL-4Rα, IL-13Rα1, and IL-13Rα2, we scratched confluent keratinocyte sheets and examined the expression of three IL-13 receptors using quantitative real-time PCR (qRT-PCR) and immunofluorescence techniques. Scratch injuries significantly upregulated the expression of in a scratch line number-dependent manner. Scratch-induced upregulation was synergistically enhanced in the simultaneous presence of IL-13. In contrast, scratch injuries did not alter the expression of and , even in the presence of IL-13. Scratch-induced expression was dependent on ERK1/2 and p38 MAPK signals. The expression of IL-13Rα2 protein was indeed augmented in the scratch edge area and was also overexpressed in lichenified lesional AD skin. IL-13 inhibited the expression of involucrin, an important epidermal terminal differentiation molecule. IL-13-mediated downregulation of involucrin was attenuated in IL-13Rα2-overexpressed keratinocytes, confirming the decoy function of IL-13Rα2. Our findings indicate that scratching upregulates the expression of the IL-13 decoy receptor IL-13Rα2 and counteracts IL-13 signaling. - Source: PubMed
Publication date: 2019/07/06
Ulzii DugarmaaKido-Nakahara MakikoNakahara TakeshiTsuji GakuFurue KazuhisaHashimoto-Hachiya AkikoFurue Masutaka