Stat3 (clone 7G8) pAb
- Known as:
- Stat3 (clonality 7G8) pAb
- Catalog number:
- ASA905756100
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Stat3 (clone 7G8) pAb
Related genes to: Stat3 (clone 7G8) pAb
- Gene:
- DNMBP-AS1 NIH gene
- Name:
- DNMBP antisense RNA 1
- Previous symbol:
- NCRNA00093
- Synonyms:
- FLJ40792, bA287G8.2
- Chromosome:
- 10q24.2
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2008-09-03
- Date modifiied:
- 2012-10-12
- 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: Stat3 (clone 7G8) pAb
Related articles to: Stat3 (clone 7G8) pAb
- Multiple myeloma (MM), the second most common hematological malignancy, is often treated with lenalidomide. However, resistance to this cornerstone therapy inevitably develops in nearly all patients, adversely affecting treatment outcomes and prognosis. To map the knowledge landscape, this study aims to analyze publication trends and identify research hotspots in lenalidomide resistance in MM. - Source: PubMed
Publication date: 2026/06/04
Li RuihuaHuang LingjuanHao ZhuanghuiZhao XueDai JinqianGao QinGao Yani - Atopic Dermatitis (AD) is a prevalent chronic inflammatory skin disorder with incompletely understood pathogenesis and limited therapeutic options. T-Lymphokine-Activated Killer Cell-Originated Protein Kinase (TOPK) is known to promote inflammation, its specific role in AD remains unclear. This study sought to elucidate the function of TOPK in AD pathogenesis and to delineate its underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/06/04
Du XiaohanShi XianshuaiHe QianYuan ZhengCui LongzhenTang BeibeiZhao ShuangLi YafangMa LeiLee Mee-HyunMalyarenko Olesya SXiao JuanjuanDuan QiuhongZhu Feng - The BCL-2 protein family controls the intrinsic apoptotic pathway through a delicate balance of pro- and anti-apoptotic members acting at the mitochondrial outer membrane. Anti-apoptotic proteins BCL-2, BCL-XL, MCL-1, BCL-W, and BCL2A1 (BFL-1) function as critical survival factors whose dysregulation contributes to cancer development and therapeutic resistance. This review systematically examines the multilayered regulatory mechanisms governing these proteins, including transcriptional control by NF-κB, STAT3/5, and HIF-1α; post-transcriptional regulation through alternative splicing and microRNAs; and post-translational modifications that determine protein stability and function. The clinical success of venetoclax, a selective BCL-2 inhibitor, has established BCL-2 family targeting as an effective therapeutic strategy and fundamentally changed the management of chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML). However, therapeutic challenges persist: resistance emerges through MCL-1 upregulation, BCL-2 mutations, and metabolic reprogramming; BCL-XL inhibition causes dose-limiting thrombocytopenia; and MCL-1 inhibitors face class-wide cardiac toxicity. Emerging strategies to overcome these limitations include tissue-selective proteolysis-targeting chimeras (PROTACs) and antibody-drug conjugates (ADCs) enabling tumor-targeted delivery, next-generation inhibitors that overcome resistance mutations, and biomarker-guided patient selection. This review provides an integrated overview of the regulatory mechanisms and evolving therapeutic strategies targeting anti-apoptotic BCL-2 family proteins, outlining both prominent successes and unresolved challenges. - Source: PubMed
Publication date: 2026/06/03
Wang ZheTang MutianKonopleva Marina - Patients with signal transducer and activator of transcription 3-related hyper-IgE syndrome (STAT3-HIES) complicated by invasive pulmonary aspergillosis typically show rapid disease progression, a tendency toward systemic dissemination, prolonged treatment courses, frequent relapse after therapy, and a poor prognosis. Some patients with STAT3-HIES also develop allergic bronchopulmonary aspergillosis (ABPA). Conventional treatment of ABPA relies primarily on glucocorticoids; however, because patients with STAT3-HIES already have immune deficiency, glucocorticoid therapy may further suppress immune function. New therapeutic strategies using biologic agents for STAT3-HIES complicated by ABPA are urgently needed. We report a patient with STAT3-HIES complicated by invasive pulmonary aspergillosis and ABPA who was treated with oral posaconazole, bronchoscopic instillation of amphotericin B, and omalizumab. Afte treatment, the patient's cough was alleviated, pulmonary function improved, mucus plugs resolved, and serum total IgE decreased significantly. By summarizing this case together with a literature review, we hope to raise awareness of STAT3-HIES complicated by invasive pulmonary aspergillosis and ABPA and to improve future treatment strategies. - Source: PubMed
Xu W SWan Y HZhao J QMu X D - Benzalkonium chloride (BAC), a widely used disinfectant compound, has been clinically associated with granular parakeratosis (GP), yet the underlying molecular mechanisms remain poorly defined. To address this, this study integrated network toxicology, molecular docking, and molecular dynamics simulation to uncover potential targets and mechanisms underlying the skin toxicity of BAC, with further validation through in vitro experiments using human skin keratinocytes. Network toxicology analysis of public databases identified 38 overlapping candidate genes linking BAC to GP. Subsequent enrichment analysis revealed these genes were significantly involved in biological processes critical for skin homeostasis, including keratinocyte differentiation, inflammatory response, and key signaling pathways such as EGFR and JAK-STAT. Molecular docking and dynamics simulations suggested CXCR4 as a potential interacting target for BAC. This prediction was experimentally supported in human keratinocytes (HaCaT cells) using the Drug Affinity Responsive Target Stability (DARTS) assay, supporting a physical interaction between BAC and CXCR4. Functional in vitro studies demonstrated that BAC exposure induced dose-dependent cytotoxicity, impaired proliferation and migration, and disrupted intercellular tight junctions. Furthermore, BAC treatment triggered upregulation of IL-1β, IL-6, and TNF-α mRNA, and increased phosphorylation of STAT3. Most importantly, pharmacological and genetic inhibition of CXCR4 substantially mitigated all the aforementioned cytotoxic, functional, and inflammatory effects induced by BAC, and specifically blocked the activation of STAT3. In conclusion, our findings suggest that BAC exposure in keratinocytes induces barrier-related dysfunction and inflammatory responses, potentially involving CXCR4-associated STAT3 signaling. These results provide mechanistic insight into BAC-related skin toxicity and warrant further investigation in disease-relevant models. This work not only advances our understanding of the disease but also identifies a promising therapeutic target for future intervention. - Source: PubMed
Publication date: 2026/06/02
Wu MofanZhang ShuaiYan ZhenyuYang JinfangYang HuihuiLi JingHuang ZhenyaoYuan Jiali