STAT3 (Phospho_Tyr705) Antibody
- Known as:
- STAT3 (Phospho_Tyr705) Antibody
- Catalog number:
- E011045-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- STAT3 (Phospho_Tyr705) Antibody
Related genes to: STAT3 (Phospho_Tyr705) 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_Tyr705) Antibody
Related articles to: STAT3 (Phospho_Tyr705) Antibody
- PEDF has neuroprotective, anti-inflammatory, anti-oxidative stress, and anti-angiogenic actions, but its multifunctional mechanisms remain unclear. We map the developmental distribution of the PEDF receptors LR, LRP6, and ATGL in naïve and Pedf retinas, and define receptor-specific signaling using siRNA and pharmacological inhibition. These receptors are broadly expressed in retinoblasts and acquire cell-type-specific patterns during retinal maturation via PEDF-independent mechanisms. LR and LRP6 also colocalize at the outer limiting membrane (OLM). Functionally, PEDF activates AKT, STAT3, ERK, and p38 and suppresses β-catenin in both HUVEC and ARPE-19 cells, while mTOR activation remains receptor-independent. LR and LRP6 couple PEDF to STAT3 and β-catenin in HUVECs, whereas in ARPE-19 cells LR links PEDF to AKT/STAT3/ERK and LRP6 to AKT/β-catenin. ATGL inhibition abolishes PEDF-induced AKT/STAT3/ERK/p38 signaling in both cell types. A 17-mer PEDF mimetic (Ppx) recapitulates these effects. These findings help define a framework for PEDF pleiotropy and highlight the OLM as a therapeutic interface. - Source: PubMed
Publication date: 2026/05/09
Yu ZihaoZhang MingliangRen ChangjieZhang XiaominBarnstable Colin JTombran-Tink JoyceLi Xiaorong - Psoriasis is a chronic skin disease characterized by keratinocyte hyperproliferation and inflammation, largely driven by the cytokines IL-22 and interferon (IFN)-γ. These cytokines activate the signal transducer and activator of transcription (STAT) 3 and STAT1 molecular pathways, leading to abnormal proliferation, impaired differentiation, and increased production of inflammatory mediators in keratinocytes. While the IL-22/STAT3 pathway primarily promotes de-differentiation in keratinocytes, IFN-γ/STAT1-3 signaling induces pronounced inflammation, despite exerting antiproliferative effects on these cells. Recent research has highlighted the role of serine/glycine metabolism in the pathogenesis of psoriasis, by supporting T cell and keratinocyte proliferation. Furthermore, pharmacological inhibition of serine catabolism through targeting serine hydroxymethyltranferase (SHMT)1/2 enzymes reduced the infiltration of inflammatory cells in the skin of the imiquimod-induced mouse model of psoriasis. This study investigates the role of serine catabolism in psoriasis, focusing on its influence on keratinocyte proliferation and inflammation. We examined how pharmacological inhibition of SHMT1/2, mediated by a folate-competitive cell-permeable inhibitor Serine Hydroxymethyltransferase INhibitor 1 (SHIN1), affects keratinocyte proliferation and inflammatory signaling pathways in response to psoriasis-associated cytokines IL-22 and IFN-γ, using both in vitro and ex vivo models of the disease. We found that SHIN1 reduced keratinocyte proliferation, particularly under IL-22 stimulation, and restored differentiation in ex vivo psoriasis skin explants by reversing the effects of IL-22. SHIN1 also inhibited IFN-γ-induced expression of pro-inflammatory genes (e.g., CXCL10, CXCL9, CCL5, CCL2, IL-6) and reduced STAT3 activation, with only modest effects on STAT1 and extracellular signal-regulated kinase 1/2 activation. In psoriasis explants, SHIN1 decreased the expression of Ki67, Keratin 16, and pro-inflammatory cytokines including IL-17A, IL-22, and IFN-γ. These findings support the therapeutic potential of SHIN1 as a metabolism-targeted agent for psoriasis and other cytokine-mediated skin disorders, providing a rationale for further exploration of novel treatment strategies. - Source: PubMed
Publication date: 2026/05/08
Mercurio LauraDi Francesco ValentinaSergio SimoneMorelli MartinaScarponi ClaudiaMadonna StefaniaPallotta SabatinoMancini MaraCappello AngelaCandi EleonoraAlbanesi Cristina - - Source: PubMed
Publication date: 2026/05/06
Shi YongqiangSong KairongZhou WenmingDong YanboSong WeiRan RuiZhao GuanghaiZhou KaishengNan WeiZhang Haihong - Tetramine poisoning commonly leads to epilepsy, with complex underlying mechanisms and poor treatment outcomes. This study aimed to explore the mechanisms of epilepsy induced by tetramine poisoning via network toxicology and molecular docking approaches. Tetramine poisoning targets were obtained from the SuperPred database, whereas epilepsy-related gene targets were identified through the GeneCards and OMIM databases. The intersection of tetramine targets and epilepsy-related genes revealed candidate targets. A proteinprotein interaction (PPI) network for these candidate targets was constructed via the String platform, after which the core functional modules were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted via the Metascape platform. Additionally, a targetpathway network involving Tetramine and brain injury was constructed via Cytoscape 3.8.2 software, enabling network topology analysis and screening of key components and targets. The results found that a total of 118 candidate targets for tetramine-induced epilepsy were identified. Pathway enrichment analysis indicated that tetramine-induced epilepsy is likely associated with the HIF-1, PI3K-Akt, Ras, Toll-like receptor, chemokine, and neurotrophin signaling pathways. The core targets include SRC, STAT3, HSP90AB1, MMP9, and HIF1A. To verify the above findings experimentally, this study established an epilepsy rat model by intragastric administration of different doses (0.1, 0.25, 0.5mg/kg) of tetramine. The seizure behavior was evaluated using the Racine scoring system, and hippocampal tissues were collected for subsequent tests. Real-time fluorescence quantitative PCR and Western Blot were used to detect the mRNA and protein expression levels of five core targets, as well as the phosphorylation levels of STAT3, SRC, Akt, and ERK. Immunofluorescence staining was used to observe the expression and distribution of p-STAT3 and HIF1A in brain tissues, and HE staining was used to assess the histopathological changes. The results showed that tetramine induced severe epileptic seizures in a dose-dependent manner. At the same time, the mRNA and protein expression levels of core targets HIF1A, MMP9, HSP90AB1, SRC, and STAT were all upregulated, and the phosphorylation levels of STAT3, SRC, Akt, and ERK were increased. Immunofluorescence and HE staining further confirmed the protein activation and pathological changes induced by tetramine.Network toxicology methods suggest that tetramine may induce epilepsy through multiple targets and signaling pathways. The above experimental results have preliminarily verified the key targets for network toxicology identification. However, the specific mechanism still needs to be further studied and confirmed. - Source: PubMed
Publication date: 2026/05/06
Liu Ming-WeiPeng Hui-deCun Yu-FangGao Shu-JiZhu Yan-LinLi XuanLi Cai-Rui - Cryptococcus neoformans (C. neoformans), an opportunistic fungal pathogen with a worldwide distribution, is responsible for fatal meningitis in immunocompromised and immunocompetent populations. Extracellular vesicles (EVs) derived from C. neoformans embody bioactivities that contribute to fungal interaction and survival. In the present study, we demonstrated that EVs from the encapsulated strain H99 increased CD44 expression while decreasing occludin expression. In contrast, EVs from acapsular strains were ineffective in CD44 and occludin expression. Furthermore, we discovered that H99 EVs could induce the formation of neutrophil extracellular traps (NETs). Mechanistically, the inhibition of PAD4 and p65 and the use of an NADPH inhibitor reduced the formation of NETs induced by H99 EVs. However, Δcap59 EVs and Δcap67 EVs failed to induce NETs. Moreover, NETs induced by H99 EVs disrupted tight junctions (TJs) in brain endothelial cells (bEnd.3), leading to a reduction in the expression of claudin-5 and occludin. This disruption was accompanied by the activation of STAT3, NF-κB, and MyD88-MAPK (p38/JNK) signaling pathways. Consequently, using an in vitro blood‒brain-barrier (BBB) model, we demonstrated that H99-derived EVs and H99 EVs-induced NETs contributed to the adhesion to and penetration of brain endothelial cells by C. neoformans. In summary, we have revealed that EVs derived from C. neoformans induce the formation of NETs, potentially facilitating fungal infection by disrupting tight junctions in brain endothelial cells. - Source: PubMed
Publication date: 2026/05/06
Cai ZhenmingWu TianhaoXu QingZhang EnruiTao YuanWang TingLi YuweiYang YonglinRen DenghuaZhang Mingshun