Il11ra1-flox Mouse
一般名
Il11ra1-flox
製品ID
S-CKO-17494
背景情報
C57BL/6JCya
系統ID
CKOCMP-16157-Il11ra1-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Il11ra1-flox Mouse（カタログ番号S-CKO-17494）はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
標準的な配送方法では、少なくとも3匹のヘテロ接合体キャリアを保証しています。ホモ接合体キャリアや指定された性別の個体の繁殖サービスも利用可能です。
基本情報
系統名
Il11ra1-flox
系統ID
CKOCMP-16157-Il11ra1-B6J-VA
遺伝子名
製品ID
S-CKO-17494
遺伝子別名
NR1, GP130, Il11ra, Il-11ra, Il11ra2
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 4
表現型
アプリケーション
--
さらに
系統詳細
EnsemblトランスクリプトID
ENSMUST00000098132
NCBIトランスクリプトID
NM_001163401
ターゲット領域
Exon 4~7
有効領域の大きさ
~1.5 kb
遺伝子研究の概要
Il11ra1, encoding the interleukin-11 receptor subunit alpha-1, is crucial for interleukin-11 (IL-11) signaling. IL-11 is a pro-inflammatory cytokine of the IL-6 family, and Il11ra1 enables IL-11 to regulate pathways like ERK-AMPK-mTORC1, which are important for cellular, tissue-and organismal-level functions and are associated with ageing, metabolism, and fibrosis-related processes [1,2,3,4,5,6,7,8].
In mouse models, deletion of Il11ra1 has shown protective effects in multiple disease conditions. In aged mice, Il11ra1 deletion protects against metabolic decline, multi-morbidity, and frailty [1]. In models of non-alcoholic steatohepatitis (NASH), Il11ra1 -/- mice had reduced steatosis, fibrosis, and inflammation compared to wild-type mice [3]. In the bleomycin mouse model of pulmonary fibrosis, Il11ra1-deleted mice, whose lung fibroblasts are unresponsive to profibrotic stimulation, are protected from fibrosis [4]. In cardiovascular fibrosis, genetic deletion of Il11ra1 protects against heart and kidney fibrosis and organ failure [5]. In hepatocyte-specific models, deletion of Il11ra1 protects against liver steatosis, fibrosis, and inflammation in NASH models [6]. In acute and chronic kidney disease models, mice with TEC-specific deletion of Il11ra1 have reduced pathogenic signaling and are protected from renal injury-induced inflammation, fibrosis, and failure [7]. In acetaminophen-induced liver injury, hepatocyte-specific deletion of Il11ra1 protects against liver injury [8]. Also, nanoparticle-mediated RNA interference targeting Il11ra1 effectively inhibits HSC activation and resolves fibrosis and inflammation in NASH models [9].
In conclusion, Il11ra1 is essential for IL-11-mediated signaling. The use of Il11ra1 gene-knockout (KO) and conditional-knockout (CKO) mouse models has revealed its significant role in various disease conditions such as ageing-related pathologies, NASH, pulmonary fibrosis, cardiovascular fibrosis, and kidney diseases. These findings suggest that targeting Il11ra1 or the IL-11/Il11ra1 axis could be a potential therapeutic strategy for treating these fibrotic and age-related diseases.
References：
1. Widjaja, Anissa A, Lim, Wei-Wen, Viswanathan, Sivakumar, Carling, David, Cook, Stuart A. 2024. Inhibition of IL-11 signalling extends mammalian healthspan and lifespan. In Nature, 632, 157-165. doi:10.1038/s41586-024-07701-9. https://pubmed.ncbi.nlm.nih.gov/39020175/
2. Zhuang, Tao, Chen, Mei-Hua, Wu, Ruo-Xi, Zuo, Jun-Li, Ruan, Cheng-Chao. 2024. ALKBH5-mediated m6A modification of IL-11 drives macrophage-to-myofibroblast transition and pathological cardiac fibrosis in mice. In Nature communications, 15, 1995. doi:10.1038/s41467-024-46357-x. https://pubmed.ncbi.nlm.nih.gov/38443404/
3. Widjaja, Anissa A, Singh, Brijesh K, Adami, Eleonora, Schafer, Sebastian, Cook, Stuart A. 2019. Inhibiting Interleukin 11 Signaling Reduces Hepatocyte Death and Liver Fibrosis, Inflammation, and Steatosis in Mouse Models of Nonalcoholic Steatohepatitis. In Gastroenterology, 157, 777-792.e14. doi:10.1053/j.gastro.2019.05.002. https://pubmed.ncbi.nlm.nih.gov/31078624/
4. Ng, Benjamin, Dong, Jinrui, D'Agostino, Giuseppe, Schafer, Sebastian, Cook, Stuart A. . Interleukin-11 is a therapeutic target in idiopathic pulmonary fibrosis. In Science translational medicine, 11, . doi:10.1126/scitranslmed.aaw1237. https://pubmed.ncbi.nlm.nih.gov/31554736/
5. Schafer, Sebastian, Viswanathan, Sivakumar, Widjaja, Anissa A, Sin, Kenny Y K, Cook, Stuart A. 2017. IL-11 is a crucial determinant of cardiovascular fibrosis. In Nature, 552, 110-115. doi:10.1038/nature24676. https://pubmed.ncbi.nlm.nih.gov/29160304/
6. Dong, Jinrui, Viswanathan, Sivakumar, Adami, Eleonora, Cook, Stuart A, Widjaja, Anissa A. 2021. Hepatocyte-specific IL11 cis-signaling drives lipotoxicity and underlies the transition from NAFLD to NASH. In Nature communications, 12, 66. doi:10.1038/s41467-020-20303-z. https://pubmed.ncbi.nlm.nih.gov/33397952/
7. Widjaja, Anissa A, Viswanathan, Sivakumar, Shekeran, Shamini G, Coffman, Thomas M, Cook, Stuart A. 2022. Targeting endogenous kidney regeneration using anti-IL11 therapy in acute and chronic models of kidney disease. In Nature communications, 13, 7497. doi:10.1038/s41467-022-35306-1. https://pubmed.ncbi.nlm.nih.gov/36470928/
8. Widjaja, Anissa A, Dong, Jinrui, Adami, Eleonora, Schafer, Sebastian, Cook, Stuart A. . Redefining IL11 as a regeneration-limiting hepatotoxin and therapeutic target in acetaminophen-induced liver injury. In Science translational medicine, 13, . doi:10.1126/scitranslmed.aba8146. https://pubmed.ncbi.nlm.nih.gov/34108253/
9. Zhang, Chenshuang, Teng, Yilong, Li, Fengqiao, Xu, Xiaoyang, Zhang, Xue-Qing. 2023. Nanoparticle-Mediated RNA Therapy Attenuates Nonalcoholic Steatohepatitis and Related Fibrosis by Targeting Activated Hepatic Stellate Cells. In ACS nano, 17, 14852-14870. doi:10.1021/acsnano.3c03217. https://pubmed.ncbi.nlm.nih.gov/37490628/
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