Interleukin_11 _ IL11
- Known as:
- Interleukin_11 _ IL11
- Catalog number:
- PP1033B1
- Product Quantity:
- 25 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Interleukin_11 _ IL11
Ask about this productRelated genes to: Interleukin_11 _ IL11
- 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
Related articles to: Interleukin_11 _ IL11
- Adipocytes exhibit cellular plasticity by secreting pro-inflammatory cytokines in response to an energy excess. Here, we identify that interleukin (IL)-11 is robustly induced and secreted from adipocytes, especially beige adipocytes upon adrenergic stimulation. IL-11 inhibits adipocyte thermogenesis through binding to IL-11 receptor a (IL-11Ra) and serves as a "brake" to maintain energy homeostasis. Adipocyte-specific IL-11Ra-knockout mice exhibit enhanced whole-body energy consumption and improved glucose and lipid metabolism under a high-fat diet (HFD). Inhibition of IL-11/IL-11Ra signaling enhances sphingosine kinase 1 (Sphk1)-driven production of sphingosine-1-phosphate (S1P), thus remodeling intracellular calcium cycling in beige adipocytes. Notably, treatment with a designed peptide against IL-11Ra in obese mice effectively alleviates fat accumulation and obesity-associated disorders. Taken together, our study defines a physiological and noncanonical mechanism of beige adipocyte-derived IL-11 in energy metabolism, which may serve as a promising target for the treatment of obesity. - Source: PubMed
Publication date: 2026/05/14
Liu JiadaiGao RonghuiKang QianqianWang ZhihanPeng XueminGe JingWang WensheDeng HongyanXie YuyuZhu ZengzheYang MinHe RuiWang HuanyuLiu YulianMaretich PemaChang YongshengYang JichunKajimura ShingoPan RupingChen Yong - - Source: PubMed
Publication date: 2026/05/11
Zhou WeiSun WeiYung Mingo M HDai ShengCai YihuaChen Chi-WeiMeng YunxiaoLee Jennifer BBraisted John CXu YinghuaSouthall Noel TShinn PaulHuang XuefengSong ZhangfaChen XiuleiKai YanCai XinLi ZongzhuHao QiangCheung Annie N YNgan Hextan Y SLiu Stephanie SBarak StephanieHao JingDai ZhijunTzatsos AlexandrosPeng WeiqunPei HuadongHan ZhiyongChan David WZheng WeiZhu Wenge - IGF2BP1 stabilizes oncogenic mRNAs via m6A binding to drive lung adenocarcinoma (LUAD) progression, yet how this modification orchestrates immune evasion remains unclear. - Source: PubMed
Publication date: 2026/05/10
Xu YufenTan XiaoliLv XiaodongYang QiKe XingxingChen Wenyu - Food structure is expected to play an important role in modulating nutrient bioavailability and antioxidant activity in cereal-based foods. This study examined how semolina type [pigmented grains (Grano Mischio, GM) vs. traditional wheat (Senatore Cappelli, SC)] and the food matrix (bread vs. pasta) influence product quality, in vitro starch digestibility, antioxidant capacity, and intestinal barrier integrity of Caco-2 cells. GM-bread had lower specific volume and was harder than SC-bread, while GM-pasta showed significantly higher starch digestibility compared to SC-pasta, probably due to polyphenol-induced structure weakening. Antioxidant activity, measured by ORAC, DPPH, and ABTS assays, varied by matrix and method, with GM-pasta exhibiting higher radical scavenging capacity than GM-bread in the DPPH and ABTS assays. Caco-2 cells treated with digested GM-pasta showed increased viability, enhanced transepithelial electrical resistance, and reduced inflammatory markers (IL-1β, IL-11, NF-κB) under pro-inflammatory conditions. Overall, pigmented wheat products, particularly pasta, retain antioxidant properties upon digestion. These findings provide evidence that food processing can modulate the biological properties of raw cereal materials, laying a promising foundation for the rational design of functional foods that leverage matrix architecture to optimize the release and efficacy of bioactive compounds during digestion. - Source: PubMed
Publication date: 2026/05/03
Feliziani GiuliaTagliasco MariannaSuo XinyingPellegrini NicolettaVittadini ElenaBordoni LauraGabbianelli Rosita - Chemotherapy- and/or radiotherapy-induced oral mucositis (CRIOM) is a common complication in patients with head and neck cancer, driven largely by excessive proinflammatory cytokine signalling and treatment-associated bacterial dysbiosis. This narrative review synthesizes current mechanistic evidence and summarizes emerging therapeutic strategies targeting these pathways. Research indicates that elevated levels of IL-1β, IL-6, TNF, iNOS, and nitric oxide amplify tissue injury and ulceration, while disruption of oral and gut microbial communities, characterized by loss of beneficial commensals and enrichment of pathogenic taxa, further exacerbates mucosal inflammation. Anti-inflammatory agents, including pentoxifylline, atorvastatin, trans-caryophyllene, azilsartan, recombinant human IL-11, and low-level laser therapy have been shown in preclinical models to reduce cytokine levels and promote mucosal healing. Similarly, microbiome-targeted approaches, such as oral microbiota transplantation and multi-strain probiotic formulations, have demonstrated potential in restoring microbial balance and attenuating CRIOM severity, with current evidence including both preclinical and clinical studies. Overall, current findings highlight cytokine toxicity and dysbiosis as synergistic drivers of CRIOM and support anti-inflammatory and microbiome-modulating strategies as promising adjunctive approaches; however, further well-designed clinical studies are required to validate their efficacy and guide clinical translation. - Source: PubMed
Publication date: 2026/04/11
Abdolmohammadi PouriaAali MaralLehmann Christian