Ask about this productRelated genes to: IL11 protein (Mouse)
- 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: IL11 protein (Mouse)
Related articles to: IL11 protein (Mouse)
- Effective treatment of pulmonary diseases remains constrained by the scarcity of delivery systems capable of selective tissue targeting. Herein, we report a lung-targeting platform created through the structural repurposing of hemoglobin (Hb). Acidic heating enables a conformational shift of Hb from α-helix to β-sheet, leading to its self-assembly into fibrils (HbFs). Unexpectedly, intravenously injected HbFs exhibit rapid and specific accumulation in the lungs. Cryo-electron microscopy (cryo-EM) structure determination revealed a fibril surface rich in positively charged residues, which facilitates two key functions: selective binding to circulating platelets via a hitchhiking mechanism for lung targeting, and efficient electrostatic complexation with mRNA. In a therapeutic application, HbFs loaded with mRNA encoding an interleukin-11 single-chain fragment variable (IL-11 scFv) were administered in a murine model of bleomycin-induced pulmonary fibrosis. The formulation achieved lung-specific delivery with predominant uptake by pulmonary fibroblasts, enabling sustained local IL-11 scFv expression. Consequently, treatment significantly suppressed fibroblast activation and migration, attenuated collagen deposition, restored lung function. This work establishes HbFs as a novel protein‑based vehicle for targeted mRNA delivery, leveraging natural cellular trafficking pathways to enable localized therapy for lung disorders. - Source: PubMed
Publication date: 2026/06/12
Liu XihuaLi SaiyaWu GuodongLi ShuangjianHuang Long ShuangLi XiaoyangZhao YiguoLu WeiSun CuixiaCao QinFang YapengCao Yiping - Lung cancer is a leading cause of cancer-related mortality, with metastasis significantly reducing patient survival. Interleukin 11 (IL11), a member of the IL-6 cytokine family, has been associated with cancer progression, yet its role in non-small cell lung cancer (NSCLC) metastasis remains unclear. This study analyzed public datasets and demonstrated that IL11 is upregulated in NSCLC and correlates with lymphatic metastasis and poor prognosis. Functional assays revealed that IL11 enhances lung cancer cell migration through upregulation of matrix metalloproteinase 12 (MMP12). Mechanistically, IL11 acts via the IL11 receptor subunit alpha (IL11RA)/ IL6 cytokine family signal transducer (IL6ST) complex to activate the PI3K/Akt/NF-κB signaling pathway, which in turn drives MMP12 expression and promotes metastatic behavior. Notably, the clinically approved selective estrogen receptor modulator bazedoxifene effectively inhibited IL11-induced signaling, reduced MMP12 levels, and suppressed cancer cell migration in vitro. In an orthotopic lung cancer mouse model, IL11 knockdown significantly reduced tumor growth and intrapulmonary spread, accompanied by decreased IL11, MMP12, and phosphorylated NF-κB p65 levels in lung tissues. These findings uncover a novel IL11-driven pathway contributing to metastatic behavior in NSCLC and identify the IL11/IL11RA/IL6ST axis as a potential therapeutic target.Schematic representation of bazedoxifene-mediated suppression of IL11-induced pro-metastatic signaling in lung cancer. Non-small cell lung cancer (NSCLC) cells secrete IL11, which binds to the IL11RA/IL6ST receptor complex and activates the PI3K/Akt signaling pathway. This activation enhances NF-κB transcriptional activity, leading to upregulated MMP12 expression and promoting lung cancer cell migration. Notably, bazedoxifene effectively blocks IL11-induced PI3K/Akt activation, thereby suppressing NF-κB signaling and reducing MMP12 expression, which ultimately attenuates NSCLC metastasis. - Source: PubMed
Publication date: 2026/06/11
Lee Chiang-WenLin Shih-SenChang Tsung-MingLin Zih-ChanChiang Yao-ChangChi Miao-ChingPeng Kuo-TiFang Mei-LingLiu Ju-Fang - Improving water-use efficiency and seed yield stability under moisture deficit stress is a major challenge in cultivation. The present study evaluated -derived introgression lines (ILs) to elucidate the role of source-sink relationships in enhancing seed yield under moisture deficit stress conditions. A set of 191 ILs, along with their parental lines, was assessed under rainfed and irrigated conditions for various agromorphological and physiological traits. Results revealed that ILs consistently outperformed parents for dry matter accumulation at maturity, seed yield per plant, harvest index, flowering duration, and reproductive-stage dry matter accumulation across environments. Under moisture-deficit stress, ILs maintained comparable crop growth rate and net assimilation rate to those of parents, while exhibiting enhanced physiological plasticity under irrigated conditions. Trait association and scatterplot analyses revealed that balanced source-sink ratio and efficient dry matter partitioning in ILs were critical determinants of seed yield under rainfed conditions. Principal component analysis further demonstrated strong multivariate associations of seed yield with crop growth rate, net assimilation rate, leaf area index, reproductive dry matter accumulation, and source-sink traits, clearly differentiating superior ILs from their parents. Several introgression lines, including IL11, IL33, IL54, IL73, IL83, IL112, IL124, IL128, IL134, IL135, IL155, IL161, and IL165, emerged as promising for moisture deficit stress conditions. Overall, the study highlights that integrating physiological efficiency with source-sink traits provides a robust framework for improving drought resilience and yield stability in breeding programs through interspecific hybridization. - Source: PubMed
Publication date: 2026/05/26
Limbalkar Omkar MaharudraVasisth PrashantDhanasekaran GokulanSharma MohitMeena Mohan LalWatts AnshulChinnusamy ViswanathanSingh Naveen - Patients with cancer who are treated for tumors located in the abdominopelvic region may develop radiation proctitis. This condition is characterized by severe mucosal inflammation that can significantly impair quality of life. In the colon, it's now established that the stroma orchestrates epithelial, endothelial, and immune cell homeostasis and plays a pivotal role following an injury. A more comprehensive understanding of the underlying mechanisms responsible for digestive mucosa injury and regeneration processes would enable therapeutic targets to be identified for limiting or even treating digestive lesions caused by radiotherapy. In this work, single-cell RNA sequencing was combined with spatial transcriptomics (ST) for an in-depth characterization of colonic stromal cells, highlighting their heterogeneity, their specific functions and interactions in homeostasis, and changes they undergo following localized colon irradiation. The present study identifies the Edil3 marker, (EGF-like repeats and discoidin domains 3), that distinguishes the most abundant stromal population, alongside the previously characterized trophocytes and telocytes. We propose the term "mesitocytes", from the ancient Greek "mesítês" ("intermediary"), for this stromal subtype, in accordance with both their position along the crypt axis and their role in the BMP/Wnt gradient. After irradiation, we demonstrate the deregulation of the stromal compartment, with an increase of genes involved in immune response, angiogenesis, and regenerative epithelial process. Specifically in the ulcerated area, Edil3 mesitocytes and telocytes are no longer detected by ST. Instead, inflammation-associated fibroblasts (IAFs) emerge, characterized by a distinct transcriptomic signature, including Ereg, Igfbp5, Il11 and C3. This feature is substantiated by analysis of human transcriptomic data which underscores the significance of our findings. Cell fate analysis further clarifies the origins of IAFs, identifying Edil3 mesitocytes as their main source. Furthermore, we observe that IAFs cooperate with endothelial cells, and we also demonstrate IAF-specific molecules involvement in epithelial disruption and endothelial activation, suggesting their key role in disease progression. - Source: PubMed
Publication date: 2026/06/09
Jestin MartinDucos ClaireAmarante-Silva DiegoSquiban ClaireDemarquay ChristelleTarlet GeorgesBuard ValerieDe Roffignac LouiseFleury CarlaPetrenko NataliaDeutsch EricMondini MicheleBenadjaoud Mohamed AmineMilliat FabienMathieu Noëlle - Current barriers to achieving radical life extension include the inability to use syngeneic, youthful mesenchymal stem cells (MSCs) and the anti-regenerative effects of senescence-associated secretory phenotype (SASP) factors. We aim to overcome this by a combination approach in which senescent cell burden is reduced utilizing SenoVax™ a dendritic cell based senolytic immunotherapy combined with syngeneic pluripotent stem cell derived MSC. - Source: PubMed
Publication date: 2026/06/08
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