Proteins IL-11 , Human
- Known as:
- Proteins Interleukin-11 , Human
- Catalog number:
- C006
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins IL-11 Human
Related genes to: Proteins IL-11 , Human
- 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: Proteins IL-11 , Human
Related articles to: Proteins IL-11 , Human
- Microglia are the main targets of HIV-1 infection in the central nervous system (CNS) and are considered important contributors to chronic neuroinflammation in people living with HIV (PLWH). In this study, we investigated the mechanisms leading to inflammatory responses during acute HIV-1 infection in an adult human microglia model. - Source: PubMed
Publication date: 2026/08/14
Gaete-Argel AracellyAnanías-Sáez CatarinaRojas-Fuentes CeciliaGiraldo-Ocampo SebastianJara DanielaHernández-Díaz TomásOrtega-Orellana CamilaLópez-Palma DeliaAkiyama HisashiGummuluru SuryaramGonzález Pablo AValiente-Echeverría FernandoSoto-Rifo Ricardo - Chronic renal allograft dysfunction (CRAD) continues to limit the long-term survival of transplanted kidneys. Inflammatory cell accumulation during the early phase of CRAD may accelerate fibrotic remodeling and graft dysfunction, although the regulatory mechanisms driving this process have not been fully clarified. Interleukin-11 (IL-11) is increasingly recognized as a fibro-inflammatory mediator, but whether miRNA-dependent regulation of IL-11 participates in early CRAD-associated inflammation remains unknown. This study aimed to investigate whether miR-204-5p regulates early inflammatory injury in CRAD by targeting IL-11. - Source: PubMed
Publication date: 2026/08/11
Wang LinZhu LinPeng SaiZheng QiangZhang QinghuaChen YixinLu YiDeng Jin - Interleukin-11 (IL-11), a member of the glycoprotein-130 cytokine family, has been implicated in inflammation-associated malignancies, including pancreatic cancer, where both IL-11 and its receptors are frequently overexpressed; however, the transcriptional mechanisms that regulate IL-11 expression remain unclear. To investigate this mechanism, promoter reporter assays, electrophoretic mobility shift assays, EGR1 knockdown experiments, gene expression analyses and three-dimensional spheroid invasion assays were performed in pancreatic cancer cells. In the present study, early growth response 1 (EGR1) was identified as a key regulator of insulin-like growth factor 1 (IGF-1)-induced transcription. Promoter analyses revealed a conserved EGR1-binding sequence (EBS) within the proximal promoter that is essential for IGF-1-responsive transcriptional activation. Electrophoretic mobility shift assays demonstrated that EGR1 directly binds to this site. Functional silencing of EGR1 markedly attenuated IGF-1-induced IL-11 expression and reduced invasive behavior in a three-dimensional pancreatic cancer spheroid model. Collectively, these findings delineated an IGF-1/EGR1/IL-11 signaling axis linking growth factor-dependent transcriptional regulation to invasive phenotypes and highlighted a potential therapeutic target in pancreatic cancer. - Source: PubMed
Publication date: 2026/08/13
Choi YenaJung EuitaekHan JunekyuShin Soon Young - Inflammatory bowel diseases (IBDs) are characterized by chronic intestinal inflammation, in which inflammatory fibroblasts contribute to epithelial damage and amplification of mucosal inflammation. However, the molecular mechanisms regulating their pathogenic activity remain incompletely understood. This study investigated the role of the epigenetic reader BRD4 in the differentiation and function of IL-13RA2-expressing inflammatory fibroblasts in IBD. - Source: PubMed
Frascatani RacheleSerra Mattia AlbertoIannucci AndreaColella MarcoMaresca ClaudiaMarafini IreneLolli ElisabettaSena GiorgiaDivizia AndreaGuida Andrea MartinaSica Giuseppe SigismondoMonteleone Giovanni - Peutz-Jeghers syndrome (PJS) is a rare autosomal dominant disorder caused by germline mutations in STK11, and is characterized by gastrointestinal hamartomatous polyps, the recurrent development of which significantly impacts patients' quality of life. While stromal cells have been implicated in PJS polyp formation, their specific characteristics remain unclear. Domènech-Moreno et al identify polyp-enriched crypt top fibroblasts (pCTFs) as the pathogenic fibroblast population and demonstrate that interleukin (IL)-11, a major secretory factor produced by these cells, serves as a critical mediator linking STK11 deficiency to epithelial proliferation. The study reveals that Stk11 loss triggers IL-11 expression, which in turn reinforces the pathogenic pCTF phenotype through autocrine signaling, forming a feedforward loop. Importantly, IL-11 neutralization significantly reduces polyp formation in a faithful mouse model, providing strong preclinical evidence for therapeutic translation. This work represents a significant advance in our understanding of PJS pathogenesis and establishes IL-11 as a promising therapeutic target. Future investigations into the effects of IL-11 neutralization on established polyps will further refine the translational potential of these findings for preventive intervention strategies. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/08/19
Nishina Takashi