Mouse Interleukin 11,IL-11 ELISA KIT
- Known as:
- Mouse Interleukin 11,Interleukin-11 Enzyme-linked immunosorbent assay test KIT
- Catalog number:
- BLS0020Mo
- Product Quantity:
- 48T
- Category:
- -
- Supplier:
- bester
- Gene target:
- Mouse Interleukin 11 IL-11 ELISA KIT
Ask about this productRelated genes to: Mouse Interleukin 11,IL-11 ELISA KIT
- 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
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Related articles to: Mouse Interleukin 11,IL-11 ELISA KIT
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Tan JinyuWu XiaominHuang WeidongHe JinshenNie JingZhou LongyuanLiu ZishanWang YuLiu CaiguangLi JieZhang YaoChen MinhuMao RenXiong Shanshan - This study aims to evaluate the efficacy and safety of hetrombopag in the management of chemotherapy-induced thrombocytopenia (CIT) among patients with solid tumors, utilizing a retrospective cohort study design. - Source: PubMed
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Yuan YuanTong QiangLiu Jia-HuiKang Ye - The Consensus Molecular Subtype 4 (CMS4) of colorectal cancer (CRC) has the worst prognosis and the highest frequency of hepatic metastases. It is characterized by abundant cancer-associated fibroblasts (CAFs) in the tumor microenvironment and active TGFβ signaling, but the molecular drivers of metastasis remain unclear. Here, we show that TGFβ signaling in CRC patient-derived CAFs from the primary tumor induces production of IL-6 family cytokines, particularly IL-6 and IL-11. These cytokines stimulate hepatocytes to express myeloid chemoattractants, including SAA1, through gp130-dependent JAK/STAT signaling. This promotes neutrophil recruitment to the liver, potentially creating a pro-metastatic niche. This IL-6 family-JAK/STAT stromal signaling axis is active in both a murine model of CMS4 as well as in patients with human CRC . Combined, our data reveal that TGFβ-driven CAF signaling actively contributes to the formation of a neutrophil-dependent, pre-metastatic hepatic niche in the metastatic phenotype of CMS4 CRC. - Source: PubMed
Publication date: 2025/10/04
Harryvan Tom JAbudukelimu SubinuerStouten Imkevan der Wel Ezra JJanson Stefanus G TLenos Kristiaan JLannagan Tamsin R MWhite MarkSansom Owen JVerdegaal Els M EHawinkels Lukas J A C - Dengue is a vector-borne infectious disease, caused by dengue virus (DENV), with a rapidly increasing incidence worldwide. With no feasible, widely applicable prevention method available in the near term, the need for an effective treatment is of great importance. This systematic review aims to provide a comprehensive overview of potential antiviral, immunomodulatory, and platelet-enhancing therapies for the treatment of DENV. This systematic review was conducted according to the PRISMA guidelines. Clinical trials that investigate treatment options for DENV in the general population were included. Twenty-six studies were included, investigating length of hospital stay ( = 10), platelet count ( = 16), interleukin (IL)-6 levels ( = 4), virological log reduction (VLR) ( = 2), and non-structural (NS)-1 clearance time ( = 4). Focusing on potential antiviral agents, four studies showed a significant reduction regarding length of hospital stay, of which two used doxycycline. The most profound reduction of hospital stay was observed when doxycycline was combined with herbal extract (7.3 days vs 9.1 days). This combination was also able to achieve a significant rise in platelet count (+154.1 × 10/L vs + 66.0 × 10/L in 7 days). Immunomodulatory therapies did not demonstrate efficacy against DENV, although some evidence suggests that rupatadine may increase platelet count. The platelet-enhancing agents recombinant human IL-11, anti-rhD immunoglobulin (anti-D), and eltrombopag all showed a significant rise in platelet count. Small sample sizes make it challenging to draw definitive conclusions out of the included studies. Larger clinical trials are needed to evaluate treatments for DENV, with particular focus on doxycycline, , rupatadine, and platelet-enhancing agents. - Source: PubMed
Publication date: 2025/11/13
Aynekulu Mersha D GDuijff FLangerak THakim M SMartina BGoeijenbier MDalm V A S Hvan Lelyveld S F Lvan Gorp E C M - Faust Akl . revealed in a paradigm-shifting mechanism distinct from myeloid-driven immunosuppression, whereby glioblastoma induces T-cell apoptosis via tumor-derived IL-11, prompting astrocytes to reprogram into immunosuppressive tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) effectors, thereby establishing astrocytes as active immunomodulators. Therapeutically, herpes simplex virus type 1 (HSV-1) (anti-TRAIL) achieves a dual therapeutic effect, offering novel strategies to overcome glioblastoma (GBM)'s evasion tactics. - Source: PubMed
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