Stat1 _ Stat3 EMSA Kit
- Known as:
- Stat1 _ Stat3 EMSA Kit
- Catalog number:
- AY1404
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- Stat1 _ Stat3 EMSA Kit
Related genes to: Stat1 _ Stat3 EMSA Kit
- Gene:
- STAT1 NIH gene
- Name:
- signal transducer and activator of transcription 1
- Previous symbol:
- -
- Synonyms:
- STAT91, ISGF-3
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
- Gene:
- STAT3 NIH gene
- Name:
- signal transducer and activator of transcription 3
- Previous symbol:
- -
- Synonyms:
- APRF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: Stat1 _ Stat3 EMSA Kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit(1-Kit) 14,15-EET_DHET Hypertension ELISA Kit Related articles to: Stat1 _ Stat3 EMSA Kit
- Heart failure (HF) and non-obstructive azoospermia (NOA) are high-burden diseases that share chronic inflammation and tissue injury. Macrophages are key regulators in both conditions, yet whether a common molecular basis exists remains unclear. - Source: PubMed
Publication date: 2026/09/15
Zhao ZhengLi RongLi KaiZhang RuiTian JiaweiTeng DaZhou XiaoyanJia BaoqiYuan XianmiaoXin Hui - Cough is a prominent and often persistent manifestation of chronic bronchitis (CB) that is frequently difficult to resolve. While Qi Feng Gu Biao Granules (QFGBG) is a traditional Chinese medicine commonly used to treat CB, its pharmacological basis for CB-related cough remains unclear.This study characterized the chemical profile of QFGBG by UPLC-Q-TOF/MS, evaluated its antitussive and anti-inflammatory effects in a rat model induced by lipopolysaccharide instillation combined with cigarette smoke exposure, and integrated network pharmacology, molecular docking, Western blotting, and plasma metabolomics to explore the underlying mechanism.QFGBG reduced cough frequency, prolonged cough latency, improved body-weight gain, and decreased the lung index and wet-to-dry ratio. Histological analyses showed attenuation of lung and tracheal inflammatory injury and mucus hypersecretion. QFGBG also decreased the expression of inflammatory and cough-related factors. Network pharmacology identified 215 overlapping QFGBG-CB targets, with enrichment in inflammatory and metabolic pathways, including the AGEs/RAGE signaling pathway. Molecular docking suggested favorable binding of core components, including Formononetin, Acacetin, and Vanillin, to key targets. Western blotting confirmed that QFGBG downregulated AGEs, RAGE, p-STAT1/STAT1、p-STAT3/STAT3. Metabolomics indicated regulation of glycerophospholipid and arachidonic acid metabolism. These findings suggest that the active components of QFGBG may alleviate CB-related cough by inhibiting the AGEs/RAGE signaling pathway and regulating arachidonic acid and glycerophospholipid metabolism, thereby reducing pulmonary and neurogenic inflammation and the release of cough-related mediators. - Source: PubMed
Publication date: 2026/08/25
Fang FangGu YuanyuanLiu XinyuLiu XinyingWang YatingMeng YanliGuo YuyanZuo JunWang Weiming - Emodin, a natural anthraquinone compound, exhibits anti-inflammatory, antioxidant, and broad-spectrum anti-tumor activities. Studies have shown that Emodin can inhibit the activation and functions of various immune cells, thereby being recognized as an important immunosuppressive agent. In this study, we conducted experiments to examine the effects of Emodin on the apoptosis, differentiation, and immunosuppressive functions of myeloid-derived suppressor cells (MDSCs), as well as its impacts on the migration, proliferation, and viability of mouse pancreatic cancer H7 cells. Furthermore, we established a mouse orthotopic pancreatic cancer model to evaluate Emodin's anti-pancreatic cancer effects and its modulation of immune cell subpopulations. The results revealed that Emodin exerts anti-pancreatic cancer effects through direct inhibition of tumor cells and regulation of MDSCs, although its modulation of the immune microenvironment exhibits concentration-dependent and subset-specific characteristics. These findings suggest that combination therapy and dose optimization are crucial directions for its clinical translation. - Source: PubMed
Publication date: 2026/09/14
Shu YatingMa LiXiao WeilingLi XingyueQi XiaotianPeng Meiyu - L. (POL) has anti-inflammatory and immunomodulatory activities, but its mechanism against atopic dermatitis (AD) remains incompletely understood. 2,4-dinitrofluorobenzene (DNFB)-induced AD mice were treated orally with POL or dexamethasone for 14 days. We evaluated skin lesions, scratchizng, serum IgE, histopathology, inflammatory cytokines, skin-barrier genes, JAK/STAT phosphorylation, and fecal metabolites. POL alleviated skin lesions and pruritus, reduced serum IgE concentrations, attenuated epidermal hyperplasia and inflammatory-cell and mast-cell infiltration, and restored keratinocyte architecture. It decreased IL-4, IL-13, and IL-31 expression, increased filaggrin and loricrin expression, and inhibited JAK1, STAT1, and STAT3 phosphorylation. Untargeted metabolomics showed that POL mainly regulated unsaturated fatty acid and steroid hormone biosynthesis and restored levels of anti-inflammatory and antiallergic metabolites, including (±)18-HEPE, docosahexaenoyl ethanolamide, and dehydroepiandrosterone. These findings indicate that POL ameliorates AD by suppressing Th2 inflammation through JAK1/STAT3 signaling, correcting lipid-metabolic disturbances, and restoring skin barrier integrity. - Source: PubMed
Publication date: 2026/09/07
Yong JiangyanYang KunGe YimanLuo GuiningZhu YaohuiLuo LihuaLi JiaqiXiang XinyiDing WeijunHu Yimei - Interleukin-10 (IL-10) is classically defined as a potent anti-inflammatory cytokine that protects tissues by constraining myeloid activation and limiting inflammatory cytokine production. Yet, accumulating evidence indicates that, in defined contexts, IL-10 can also promote antitumor immunity by enhancing the fitness and cytotoxic programs of CD8 T cells and natural killer (NK) cells. Conversely, in other tumor contexts, IL-10 may reinforce immunosuppressive myeloid and regulatory programs, and the factors that determine these divergent outcomes remain incompletely understood. Although these effects converge on a common JAK1/TYK2-STAT3 signaling hub, the downstream biological outcomes are combinatorially shaped by the identity, activation, and chromatin state of the responding cell, co-engaged pathways, including STAT1, mTORC1, and NF-κB/AP, receptor abundance, feedback regulation, and the surrounding microenvironment. Recent studies suggest IL-10 can sustain cytotoxic lymphocyte function under tumor microenvironmental stress through effector programming, restraint of terminal exhaustion, mitochondrial metabolic reprogramming, and remodeling of the tumor microenvironment (TME). However, several of these mechanisms remain supported primarily by limited preclinical models and correlative human data. These advances have promoted the development of pharmacokinetically optimized IL-10 variants, tumor-targeted immunocytokines, surrogate bispecific IL-10 receptor agonists, and IL-10-armored adoptive cell therapies. Although several approaches have shown immune activation and preliminary antitumor activity in early-phase studies, pegilodecakin-the only IL-10-based agent to complete a randomized phase III oncology trial-did not improve survival in gemcitabine-refractory pancreatic cancer, underscoring the gap between pharmacodynamic activity and established clinical benefit. In this review, we synthesize mechanistic and translational advances with conflicting and cautionary evidence, discuss safety considerations associated with IL-10-based agents and IL-10-armored cell therapies, and propose a context-dependent framework for their further development based on tumor and microenvironmental features, spatiotemporal control, rational combination strategies, and candidate biomarkers. - Source: PubMed
Publication date: 2026/09/07
Zhang MinchuanLi Qi-JingLam Kong PengXu Shengli