Interleukin-11 / IL11 antibody Host Rabbit
- Known as:
- Interleukin-11 / IL11 (anti-) Host Rabbit
- Catalog number:
- 'AP20671PU-N
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Interleukin-11 / IL11 antibody Host Rabbit
Related genes to: Interleukin-11 / IL11 antibody Host Rabbit
- Gene:
- IL11 NIH gene
- Name:
- interleukin 11
- Previous symbol:
- -
- Synonyms:
- IL-11, AGIF
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2016-10-11
Related products to: Interleukin-11 / IL11 antibody Host Rabbit
Related articles to: Interleukin-11 / IL11 antibody Host Rabbit
- Twinfilin-1 (TWF1) is a cellular protein that binds actin, phosphoinositides, and capping protein. Although multiple studies have reported the tumor-regulatory role of TWF1, a comprehensive and critical review of these findings remains unavailable. This review addresses this gap by consolidating current evidence on the tumor-modulatory functions of TWF1. The literature indicates that dysregulation of TWF1 or its actin-binding activity can promote carcinogenesis by influencing interleukin-11/signal transducer and activator of transcription 3, protein kinase B, epithelial-to-mesenchymal transition, or autophagy. The mechanisms by which TWF1 regulates tumorigenesis are tissue-dependent and vary across different tissues. At least 10 microRNAs, 2 long noncoding RNAs, and 1 circular RNA have been identified as interacting with TWF1, either directly or indirectly, to regulate its expression and tumor-controlling function. High TWF1 expression has been observed in at least 8 types of solid tumors, but not in liquid cancers, highlighting its potential as a diagnostic biomarker for solid tumors. Furthermore, its increased expression in solid tumors can help predict cancer patient prognosis. However, despite these findings, the translational potential of TWF1 requires further validation through in-depth mechanistic studies and large-scale clinical trials, as current evidence is primarily derived from bioinformatics analyses, preclinical studies, or small prospective cohorts. Once the tumor-promoting role of TWF1 is confirmed, future research should then evaluate its sensitivity and suitability as a biomarker or therapeutic target. SIGNIFICANCE STATEMENTS: Twinfilin-1 (TWF1) regulates various cellular processes that contribute to solid cancer cell proliferation, metastasis, and resistance to treatment. These functions suggest that TWF1 has translational potential as both a biomarker and a therapeutic target in cancer management. - Source: PubMed
Publication date: 2026/06/04
Chong Zhi-Xiong - - Source: PubMed
Publication date: 2026/07/02
Cook Stuart A - Recent studies have highlighted the crucial role of mechanical properties in the ovarian microenvironment for ovarian function. However, the mechanisms that cause ovarian matrix stiffening during aging remain incompletely understood. Here we utilized atomic force microscopy (AFM) to demonstrate that human ovarian matrix stiffness increases with aging and in pathophysiological conditions, such as chemotherapy-induced premature ovarian insufficiency (POI), polycystic ovary syndrome (PCOS) and ovarian endometriosis. By integrating proteomic analysis of human ovarian tissue with transcriptomic profiling of human ovarian fibroblasts, we identified that IL-11, which is elevated in aging ovaries of mice, rats and humans, activates fibroblasts to secrete extracellular matrix (ECM), thereby increasing ovarian matrix stiffness. Genetic deletion of Il11ra1 in mice mitigated the increase in ovarian matrix stiffness and the decline in ovarian function associated with aging, chemotherapy-induced POI and PCOS. Single-nuclei RNA sequencing (snRNA-seq) revealed that blocking Il11ra1 reduces the proportion of activated fibroblasts. Furthermore, administration of siIl11 nanoparticles to aged mice and rats enhanced fertility and reduced ovarian matrix stiffness. Together, these findings highlight the pro-inflammatory factor IL-11 in regulating ovarian matrix stiffness. We propose that anti-IL-11 therapy represents a promising translational strategy for delaying ovarian aging. - Source: PubMed
Publication date: 2026/07/02
Wu MengZhu QingqingXiong JiaqiangTang WeichengChen DanXue LiruFeng YourongDai YunWu TongWu ChuqingGuo YicanWei SiminHuang YibaoZheng PeizheLi YutingSong YiqingDing TingWu MingfuLi ZifuRong YueguangWang WenwenLi YanDai JunWang ShixuanZhang Jinjin - Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive fibrotic interstitial lung disease mainly occurs in the elderly, presents limited therapeutic options and necessitating the development of novel drugs. Interleukin-11 (IL-11) belongs to the interleukin-6 (IL-6) family and plays a wide role in fields such as hematopoiesis, immune regulation and tumorigenesis. Recent studies have shown that IL-11 could serve as a potential target for the treatment of IPF and plays a certain role in the aging process. In this study we aims to evaluate the role and mechanism of targeted IL-11 in aging-related pulmonary fibrosis. Firstly, neutralizing antibodies targeting IL-11 were obtained through evaluation and combination of two antibodies with different epitopes can effectively alleviate pulmonary fibrosis in vivo and in vitro. Subsequently, we established pulmonary fibrosis model in aging mice and found that IL-11 was highly expressed in the serum, lung tissues and fibroblasts of fibrotic aging mice. The overexpression or functional loss of IL-11 could significantly change the profibrotic phenotype of senescent lung fibroblasts, and IL-11 neutralizing antibodies could effectively alleviate early and late pulmonary fibrosis in aging mice. Further mechanism studies have confirmed the importance of the TGF-β1/NOX4/IL-11 signaling pathway in regulating the senescence phenotype of lung fibroblasts and aging-related pulmonary fibrosis. In summary, this study elucidate the correlation between IL and 11 and pulmonary fibrosis in aging mice. Both in vitro and in vivo experiments have validated the therapeutic efficacy and molecular mechanisms of IL-11-neutralizing antibodies in pulmonary fibrosis, offering promising insights for future anti-fibrotic drug development. Abbreviations: IL-11, Interleukin-11; IPF, Idiopathic pulmonary fibrosis; TGF-β, Transforming growth factor-β; NOX4, NADPH oxidase-4; SASP, Senescence-associated secretory phenotype; ECM, Extracellular matrix; α-SMA, α-smooth muscle actin; STAT3, Signal transducer and activator of transcription 3; ERK, Extracellular regulated protein kinases; AKT, Protein kinase B; BLM, Bleomycin; WT, Wild-type; KO, Knockout; qRT-PCR, Quantitative real-time polymerase chain reaction; WB, Western blot; hAb, Humanized antibody; mAb, Monoclonal antibody; FVC, Forced vital capacity; CTGF, Connective tissue growth factor; PDGFR-α, Platelet-derived growth factor receptor-α; TNF-α, Tumor necrosis factor-α; Nrf2, NFE2-related factor 2; EMT, Epithelial-mesenchymal transition; HE, Hematoxylin and eosin; PVDF, Polyvinylidene fluoride; GAPDH, Glyceraldehyde-3-phosphate dehydrogenase; siRNA, Small interfering RNA; IL-6, Interleukin-6; MEK, Mitogen-Activated Protein Kinase Kinase; TIME, TGF-β1/IL-11/MEK/ERK; HRP, Horseradish Peroxidase; MLG, Mouse lung fibroblast cell line MLg; NCBI, National Center for Biotechnology Information; Bcl2, BCL2 apoptosis regulator; Bax, BCL2 Associated X, apoptosis regulator; MSC, Mesenchymal Stem Cell; RSK, p90 Ribosomal S6 Kinase; KD, Dissociation Constant; Nin, Nintedanib; CTL, Control; Eto, Etoposide; SA-β-Gal, Senescence-Associated β-Galactosidase. - Source: PubMed
Publication date: 2026/06/27
Miao YangHu Ya-YueXu LiMeng Ling-XinYang YueLiu Zhi-GangYang Zhong-YiLiu Xue-ZeLiu Yu-MingJiao RanXu Ai-GuoGu Xiao-TingZhou Hong-GangLi Xiao-He - Asthma is characterized by persistent airway epithelial dysfunction and remodelling of the reticular basement membrane (RBM). In healthy airways, the RBM is primarily composed of the extracellular matrix (ECM) proteins laminin and collagen-IV, but in remodelled asthmatic airways, the RBM has increased deposition of collagen-I, -III and fibronectin. Here, we systematically compared the effects of collagen-I, -III, -IV, fibronectin, laminin, and bovine serum albumin (BSA) control on bronchial epithelial cells (BECs) from six healthy controls and seven individuals with asthma. Epithelial attachment, spreading and barrier function were assessed in real time over 72 h using electrical cell-substrate impedance sensing. Cell culture supernatants were analyzed for release of epithelial cytokines, thymic stromal lymphopoietin (TSLP), interleukin (IL)-6, IL-8, and IL-11 using ELISA. BECs from both control and asthma donors had faster cell attachment, spreading, and barrier formation on collagen-I, -III, -IV, and fibronectin compared to laminin and BSA. BECs from both control and asthma donors cultured on collagen -I and -III produced more TSLP, but had no effect on IL-6, IL-8, and IL-11 expression. In summary, remodelling of the RBM in asthma may promote epithelial barrier formation whilst simultaneously enhancing epithelial-derived Th2 inflammation through increased TSLP release. - Source: PubMed
Publication date: 2026/06/10
Hsieh AileenBarker-Mulleder JennaYang Chen XiFouadi MayHackett Tillie-Louise