Ask about this productRelated genes to: IL11 antibody
- 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 antibody
Related articles to: IL11 antibody
- BBT-059 is a long-acting PEGylated interleukin-11 (IL-11) analog that is believed to have hematopoietic-promoting and anti-apoptotic properties, making it an ideal candidate for further development as a potential radiation medical countermeasure (MCM) for the hematopoietic acute radiation syndrome (H-ARS). The efficacy of BBT-059 efficacy has been previously established in an H-ARS murine model and in a nonhuman primate (NHP) model through pharmacokinetic and pharmacodynamic (PK/PD) studies. In the current study, a total of 12 naïve NHPs (rhesus macaques) were administered a single 37.5 µg/kg, 75 µg/kg, or 150 µg/kg dose of BBT-059 (n = 4 animals per group) subcutaneously and monitored for 21 days post-administration. To further evaluate the safety profile of BBT-059 and better understand its mechanism of action, proteomic analyses were performed to assess the impact of BBT-059 on proteins, pathways, and any dose-dependent differences. Blood samples were collected and serum was isolated and analyzed using trapped ion mobility spectrometry time-of-flight mass spectrometry (timsTOF-MS). Statistically significant time-dependent changes were present in all dose groups when comparing pre-administration to post-administration samples, peaking around 3 days post-administration and reverting to near-normal levels by the end of the study period. Any dose of BBT-059 triggered a robust, acute-phase proteomic response characterized by an increase in platelet and neutrophil counts, elevated IL-6 expression, and an activation of the neutrophil degranulation and platelet activation, signaling and aggregation pathways. Taken together, these observations suggest that BBT-059 has a good safety profile for further development as a radiation MCM. - Source: PubMed
Publication date: 2026/05/18
Carpenter Alana DMiranda Issa MelendezLi YaoxiangPetrus Sarah AKandhavelu JeyalakshmiWise Stephen YFatanmi Oluseyi OFam Christine MCarlson Sharon JCox George NCheema Amrita KSingh Vijay K - Given the post-mitotic nature of podocytes, adapting to both physiological and pathological stress is crucial to prevent podocyte loss. An important component of maintaining cellular homeostasis are lysosomes, which are membrane-bound organelles responsible for degradation and recycling of damaged organelles and other macromolecules. Lysosome impairment has been shown to cause cellular and organ dysfunction, highlighting its crucial role in homeostasis. - Source: PubMed
Publication date: 2026/05/18
Bunda PatriciaTian XuefeiNagata SoichiroLerner GabrielMedina-Rangel PaulinaGu JianleiZhao HongyuGreene LoisFerguson ShawnInoue KazunoriIshibe Shuta - 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