IL11 protein, Native & Recombinant Proteins
- Known as:
- IL11 protein, Native & Recombinant Proteins
- Catalog number:
- 30R-2167
- Product Quantity:
- 5 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- IL11 protein Native & Recombinant Proteins
Related genes to: IL11 protein, Native & Recombinant Proteins
- 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, Native & Recombinant Proteins
Related articles to: IL11 protein, Native & Recombinant Proteins
- 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 - IL-11, a novel target for drug development, has been associated with several fibroinflammatory diseases including thyroid eye disease (TED), where it plays an important role in signaling to stromal cells activating multiple intracellular pathways. In TED patient tissue, IL-11 is elevated and stimulates multiple effects important in disease progression, including the production of proinflammatory cytokines, hyaluronic acid (HA) and fibrotic markers. LASN01, a potent antibody to IL-11 receptor, inhibits these effects and is a potential therapeutic agent for TED. Teprotumumab, an antibody to IGF-1 receptor, inhibits HA production and adipogenesis and is effective in reduction of proptosis. Activation of the IGF-1 and IL-11 pathways in TED tissue induces the expression of fibroinflammatory genes regulated by LASN01 and lipid biosynthetic genes regulated by Teprotumumab. Clinical studies show that LASN01 is well tolerated and in a placebo-controlled phase II trial in TED, LASN01 resulted in a statistically significant resolution of clinical activity score (CAS) in 88% of treated patients (p = 0.028), but had lesser effects on proptosis. The data supports the importance of IL-11 biology in fibroinflammatory disease and that IL-11 receptor is a pharmacologically active target for drug development. - Source: PubMed
Publication date: 2026/05/02
King David JSwaney James SRich CadmusJun H ToniVasquez YasminGeller ShiraChidester ChristineChai MerrickElliott EricWitherden DeborahHershoff HannahKafi AaryaStrauwald AmyKossler Andrea LSilkiss Rona ZOester AlanGarrido-Hermosilla Antonio MMalik MohsanKikkawa Don OFardis Maria - Systemic sclerosis (SSc) is a multi-organ autoimmune disease characterized by fibrosis of the skin and internal organs. Interstitial lung disease (ILD) is a major complication and leading cause of mortality in SSc. Transforming growth factor-β (TGF-β) has been implicated as a central mediator of fibrosis; however, while TGF-β1 has been extensively studied, the roles of TGF-β2 and TGF-β3 remain incompletely defined. Here, we systematically compared the effects of TGF-β1, TGF-β2, and TGF-β3 in dermal and lung fibroblasts, evaluating extracellular matrix synthesis and contraction, cytokine secretion, proliferation, and myofibroblast differentiation. TGF-β2 and TGF-β3 induced greater profibrotic cytokine release of Interleukin (IL)-6 and IL-11 and increased collagen-I and fibronectin synthesis compared with TGF-β1 in dermal and lung fibroblasts (all < 0.05). TGF-β2 and TGF-β3 stimulated greater collagen-I contraction in dermal fibroblasts ( < 0.05), but greater myofibroblast differentiation in lung fibroblasts ( < 0.05). The TGF-β isoforms did not affect proliferation. All TGF-β isoforms activated SMAD2/3 signalling; however, TGF-β2 and TGF-β3 reduced expression of TGF-β Receptor II and the inhibitory regulator, SMAD7. In summary, TGF-β2 and TGF-β3 have a more pronounced profibrotic effect than TGF-β1 on dermal and lung fibroblast functions, making them potential targets for treatment for skin and lung fibrosis in diseases such as SSc. - Source: PubMed
Publication date: 2026/04/10
Badyal RaveenKohlen BrandonKeen Kevin JDunne James VHackett Tillie-Louise - Lung adenocarcinoma (LUAD) is the main histologic subtype of lung cancer, and its incidence is on the rise. However, since the vast majority of patients are already in advanced stages at the time of diagnosis, their 5-year survival rate is only 15%, so it is urgent to explore the mechanism of the development of LUAD and improve the survival time of patients. Interleukin-11 (IL-11), a member of the IL-6 cytokine family, has an influential role in the development and progression of a variety of tumors, but the specific molecular mechanisms that promote the malignant progression of LUAD are unknown. Here, we found that the IL-11-induced activation of Akt, Erk, and STAT3 could be inhibited by knocking out the expression of Gαi1/3. In contrast, overexpression of Gαi1/3 could enhance IL-11-induced signaling. The binding of Gαi1/3 to GP130 mediates IL-11-induced downstream activation of Akt-mTOR, Erk, and STAT3, which requires recruitment of Grb2-associated binding protein 1 (Gab1). In LUAD cells, shGαi1/3 inhibited cell growth, proliferation, and migration as well as blocked the tumor-promoting ability of IL-11. However, overexpression of Gαi1/3 enhanced the IL-11-induced cell growth, proliferation, and migration. ShGαi1/3 also inhibited the proliferation of LUAD cells in vivo. Overall, the findings of this study demonstrate the Gαi1 and Gαi3 are critical for IL-11 signal transduction. Moreover, we reveal that Gαi1 and Gαi3 are highly expressed and associated with poor overall survival in lung adenocarcinoma and may thus act as potential therapeutic targets in LUAD. These results provide a novel therapeutic strategy for LUAD patients with upregulated IL-11 expression. - Source: PubMed
Publication date: 2026/04/25
Luo GaomengHu WenxuanYang JianLu ZhengCui YuanZeng WeibiaoDing HaoLi QifanChen ZhikeTong XinDing ChengXu ChunZhao Jun