STAT3 (Phospho_Ser727) Antibody
- Known as:
- STAT3 (Phospho_Ser727) Antibody
- Catalog number:
- E011046-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- STAT3 (Phospho_Ser727) Antibody
Related genes to: STAT3 (Phospho_Ser727) Antibody
- 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 (Phospho_Ser727) Antibody
Related articles to: STAT3 (Phospho_Ser727) Antibody
- Alyssin is an isothiocyanate found in cruciferous plants, and it has been reported to have physiologically active effects. However, there have been no attempts to use alyssin for the treatment of periodontitis, and there are no reports investigating the effects of alyssin on periodontal tissue component cells. In this study, experiments were conducted to determine whether alyssin has an anti-inflammatory effect on human periodontal ligament cells. - Source: PubMed
Publication date: 2026/05/11
Hosokawa IkukoHosokawa YoshitakaOkamoto RisaOzaki KazumiHosaka Keiichi - Triple negative breast cancer (TNBC) is an aggressive subtype associated with poor prognosis and limited therapeutic options. Epigenetic changes contribute to TNBC tumorigenesis, and histone deacetylase inhibitors (HDACi) have emerged as promising therapeutic agents. However, their efficacy as monotherapy in solid tumors remains limited. Recent evidence highlights their immunomodulatory potential, supporting the development of combination strategies. We investigated the effect of the HDACi suberoylanilide hydroxamic acid (SAHA) on cell viability and immunogenic cell death (ICD), as well as its combinatory potential with a SOCS3 peptidomimetic (KIRCONG chim PEG), designed to inhibit STAT3 phosphorylation (pSTAT3), in TNBC cell lines. SAHA reduced TNBC cell viability and, at its IC, induced ICD hallmarks in MDA-MB-231 cells, including ATP release, calreticulin surface exposure, and increased HMGB1 levels, accompanied by enhanced IL-6 secretion. In contrast, MDA-MB-468 cells showed limited ICD features under the same conditions. The higher IL-6 secretion observed in untreated MDA-MB-231 cells was associated with lower basal SOCS3 expression compared to MDA-MB-468 cells. Given the potential role of IL-6/JAK/STAT3 signaling in limiting HDACi efficacy, SAHA was combined with the SOCS3 peptidomimetic KIRCONG chim PEG. In MDA-MB-231 cells, co-treatment reduced pSTAT3 levels and increased BAK expression. Moreover, the combination shifted the IC of SAHA, indicating enhanced sensitivity to sub-toxic concentrations. Conditioned media from co-treated MDA-MB-231 cells promoted CD4T cell activation, as shown by increased HLA-DR and CD69 expression. Overall, these findings indicate that SOCS3 functional replacement enhances SAHA anti-cancer and immunogenic effects in IL-6 high TNBC cells, supporting a context-dependent combinatory strategy targeting the IL-6/STAT3 axis. - Source: PubMed
Publication date: 2026/05/08
Castellano GiulianoBucciero CandidaCugudda AlessiaLa Manna SaraMarasco DanielaPortella GiuseppeMalfitano Anna Maria - Phthalate esters (PAEs) are widely used in medical-grade polyvinyl chloride materials and may contribute to inflammatory injury under medical-device-relevant exposure conditions. However, the shared molecular targets linking different phthalates to multiple organ dysfunction syndrome (MODS)-related pathological processes remain unclear. Here, an integrative network toxicology approach was used to identify shared candidate inflammatory targets of diethyl phthalate (DEP), dimethyl phthalate (DMP), and dioctyl phthalate (DOP) within a MODS framework, with focused analyses of three clinically relevant MODS-related syndromes: sepsis, acute kidney injury (AKI), and acute respiratory distress syndrome (ARDS). Compound- and disease-associated targets were integrated to construct interaction networks, identify hub genes, and perform pathway enrichment and molecular docking analyses. To provide representative experimental support, di- (2-ethylhexyl) phthalate (DEHP) was selected for in vitro validation in A549, HK-2, and RAW264.7 cells. Network analysis identified recurrent candidate inflammation-related targets, with STAT3, PTGS2, and TLR4 repeatedly prioritized across the MODS-related syndrome analyses. Acute 24 h DOP/DEHP exposure reduced cell viability, increased apoptosis, elevated IL-6, TNF-α, IL-1β, and IL-18 secretion, and was associated with increased expression of TLR4, STAT3, and PTGS2 in all three cell models. These findings identify shared candidate inflammatory targets networks of representative phthalate plasticizers in MODS-related syndromes and provide hypothesis-generating evidence supporting conserved inflammatory responses to representative DOP/DEHP exposure. - Source: PubMed
Publication date: 2026/05/08
Song LinHe AifengJiang WeiLiu KeMa JingyiWang JingShi KeranYu JiangquanZheng Ruiqiang - Ectomesenchymal stem cells (EMSCs) are critical for craniofacial bone development, and low-affinity nerve growth factor receptor (LNGFR) is closely associated with their stemness. However, the specific role of LNGFR in EMSC osteogenesis remains unclear. Here, we investigated this using Lngfr knockout (lngfr) mice and demonstrated that lngfrEMSCs exhibited decreased proliferation, migration, and osteogenic differentiation capacities in vitro. Furthermore, impaired skeletal development and reduced mineralization were observed in lngfr fetal mice in vivo. Circular RNA (circRNA) sequencing identified the growth hormone (GH) pathway as a key factor involved in LNGFR-regulated osteogenesis of EMSCs. Co-immunoprecipitation (Co-IP) assays further confirmed the interaction between LNGFR and growth hormone receptor (GHR). lngfrsuppressed GHR expression and Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) phosphorylation, leading to downregulation of the GH/insulin-like growth factor 1 (IGF-1) signaling pathway. Modulation of the JAK/STAT pathway affected osteogenesis, while exogenous GH rescued the osteogenic defects via the GHR/JAK-STAT/IGF-1 axis. Collectively, these findings demonstrated that LNGFR promoted EMSC osteogenesis by activating the GHR/JAK-STAT/GH-IGF-1 signaling axis, providing new insights into craniofacial development and regenerative medicine. - Source: PubMed
Publication date: 2026/05/09
Wang KeyuZeng XiaokeZhang YaoguangZou YanhuiYe JiaqiZhao YekeJin HaoyangZhang JiajunNie XinCheng Gu - Growth differentiation factor 15 (GDF-15), a stress-responsive member of the transforming growth factor-β (TGF-β) superfamily, is consistently upregulated in multiple solid tumors and closely linked to poor clinical outcomes. This review offers a systematic overview of the pleiotropic functions and principal signaling pathways of GDF-15 in solid malignancies. Within the tumor microenvironment (TME), GDF-15 fuels tumor progression by promoting proliferation, sustaining stemness, remodeling metabolism, and conferring therapy resistance via the TGF-β, Leukemia Inhibitory Factor (LIF)-Signal Transducer and Activator of Transcription 3 (STAT3), and AKT pathways. Notably, GDF-15 orchestrates an immunosuppressive TME by limiting T cell infiltration and expanding regulatory T cells, thereby facilitating immune evasion and resistance to immune checkpoint inhibitors (ICIs). Systemically, GDF-15 contributes to cancer cachexia through activation of the brainstem glial-cell-line-derived neurotrophic factor family receptor α-like (GFRAL)-rearranged during transfection (RET) receptor axis. Accumulating preclinical evidence positions GDF-15 as a promising therapeutic target, particularly for mitigating cachexia and potentiating immunotherapy. However, the context-dependent and dualistic nature of GDF-15 signaling, varying with tumor type, microenvironment, and disease stage, poses substantial hurdles for clinical translation. Future efforts should focus on deciphering the molecular determinants underlying GDF-15's functional duality, paving the way for precise, context-tailored intervention strategies. - Source: PubMed
Publication date: 2026/05/09
Aishanjiang DilinaerAbulajiang YiliminuerSaidula ReziyaAbudusalam KaderyaMusha Kadierjiang