Stat3 (phospho_Tyr705) Rabbit pAb
- Known as:
- Stat3 (phospho_Tyr705) Rabbit pAb
- Catalog number:
- ASAKAP-TF022C
- Product Quantity:
- 25 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Stat3 (phospho_Tyr705) Rabbit pAb
Related genes to: Stat3 (phospho_Tyr705) Rabbit pAb
- 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) Rabbit pAb
Related articles to: Stat3 (phospho_Tyr705) Rabbit pAb
- Secondary injury after spinal cord injury (SCI) is sustained by coupled oxidative stress and inflammation, which drives neuronal apoptosis and bioenergetic failure. Here, a cascade-responsive Zn-centered nanoassembly (Zn-PC/PA@Gel) is constructed through stepwise coordination among Zn, procyanidin (PC), and polyarginine (PA) to form a core-shell architecture with a Zn-procyanidin core (Zn-PC) and a Zn-polyarginine shell (Zn-PA). In a reactive oxygen species (ROS) rich injury microenvironment, oxidation of guanidino groups in the polyarginine shell enables in situ nitric oxide (NO) release and weakens Zn coordination, triggering controlled shell disassembly for early modulation of local inflammation and tissue microenvironment. The subsequent release of PC and Zn provides continuous antioxidant protection. Zn further restores mitochondrial quality control by regulating the STAT3-FOXO3a-SOD2 axis, thus enhancing mitochondrial autophagy, enhancing endogenous antioxidant defense, and restoring mitochondrial homeostasis and energy metabolism. In a mouse spinal cord contusion model, Zn-PC/PA@Gel mitigated inflammation and oxidative stress, alleviated the burden of mitochondrial dysfunction, protected neurons, and promoted motor recovery, resulting in a Basso Mouse Scale (BMS) score of 7.0 on day 28. Overall, these results support Zn coordinated cascade therapy nanoassembly, which combines microenvironmental regulation with mitochondrial homeostatic recovery to reduce secondary injury after SCI and promote locomotor improvement. - Source: PubMed
Publication date: 2026/06/29
Xiang ChunyuHe XiaodongGuo FengshuoLuo HaowenHe LiuminLiu WanguoGu Rui - Emerging evidence suggests dietary interventions regulate inflammatory signaling through gut microbiome modulation, yet their therapeutic potential in radiation-induced intestinal injury (RIII) remains underexplored. This study demonstrates that ketogenic diet (KD), a high-fat and low-carbohydrate dietary regimen, exerts protective effects against RIII through dual mechanisms involving microbial regulation and inflammatory pathway inhibition. Using high-salt diet (HSD) as a dietary control, KD significantly attenuated intestinal inflammation by downregulating pro-inflammatory cytokines while enhancing barrier integrity through tight junction protein upregulation in radiation-exposed murine model. 16S rDNA sequencing showed KD enriched Akkermansia and reduced Enterobacteriaceae, whereas HSD exhibited inverse patterns. Mechanistically, RNA sequencing revealed that KD uniquely suppressed the JAK2/STAT3 pathway in RIII mice. In vitro studies demonstrated that β-hydroxybutyrate, a key ketone metabolite, effectively suppressed RORγt expression and subsequent downregulation of IL-17A gene transcription via the inhibition of JAK2/STAT3 pathway, thus mitigate inflammatory damage. Fecal microbiota transplantation validated that KD-modified microbiome directly inhibited JAK2/STAT3 signaling activation, as well as the downregulation of RORγt and IL-17A. These findings establish KD as a promising dietary strategy mitigate acute RIII through synergistic modulation of gut microbiota and inflammatory signaling, providing novel insights into nutritional approaches targeting microbial-host crosstalk in radiation injury. - Source: PubMed
Publication date: 2026/06/30
Yang JingjingLing ZhiZhou MingTao MingyangMao JingxianGuo HuaijuanWang JiaxinQu XiaoWang YingZhu YefeiZhang KunYan Xuebing - Astrocytes, long considered supportive cells of the central nervous system (CNS), have critical roles in innate immunity. This Review explores immune signaling pathways in astrocytes, including pattern recognition through Toll-like receptors, nucleic acid sensors and inflammasomes. These pathways enable the detection of danger signals and initiate protective responses and endogenous innate immune functions. Downstream signaling pathways, including the interferon, NF-κB and STAT3 pathways, mediate astrocyte reactivity and drive cytokine secretion, antiviral responses, phagocytosis and many other immune functions. While these responses are crucial for CNS health, their dysregulation can contribute to chronic inflammation and neurodegeneration in conditions such as Alzheimer's disease, Parkinson's disease, multiple sclerosis and amyotrophic lateral sclerosis. Additionally, astrocytes exhibit regional heterogeneity in their immune behaviors, which may influence disease trajectories. We highlight unresolved questions regarding the immune functions of astrocytes, their interplay with professional immune cells and their dual protective and pathological roles. - Source: PubMed
Publication date: 2026/06/29
Guo Amy XFisher Theodore MComandante-Lou NatachaDe Jager Philip LLiddelow Shane A - Ovarian cancer (OC) remains the most lethal gynecologic malignancy, with approximately 75% of patients experiencing recurrence within 18-24 months and facing poor clinical outcomes. Accumulating evidence demonstrates that circular RNAs (circRNAs) play crucial roles in OC development and that ferroptosis serves as a novel tumor suppressor mechanism. This study aimed to elucidate the functional role and underlying molecular mechanisms of circ-E2F3 in OC progression. We identified significant upregulation of circ-E2F3 (2-3.5 fold increase) and downregulation of miR-1305 (0.3-0.7 fold decrease) in OC cells compared to normal controls. Circ-E2F3 knockdown induced ferroptosis and significantly inhibited proliferation and invasion capabilities in OC cells. Furthermore, bioinformatics analysis combined with dual-luciferase reporter, RNA pull-down, and AGO2-RIP assays demonstrated functional interactions between circ-E2F3 and miR-1305, as well as between miR-1305 and signal transducer and activator of transcription 3 (STAT3). Rescue experiments showed that the tumor-suppressive effects of circ-E2F3 knockdown were partially reversed by miR-1305 silencing or STAT3 overexpression. Collectively, our findings demonstrate that circ-E2F3 upregulates STAT3 expression by sequestering miR-1305, thereby relieving miR-1305-mediated suppression of STAT3 and subsequently promoting the malignancy in OC cells. These results suggest that targeting the circ-E2F3/miR-1305/STAT3 axis may represent a promising therapeutic strategy for OC treatment. - Source: PubMed
Publication date: 2026/06/29
Li MengyingLai Limei - Glioblastoma (GBM) exhibits remarkable cellular heterogeneity, but the functional roles of distinct tumor subpopulations remain incompletely understood. - Source: PubMed
Publication date: 2026/06/29
Li JiaomingZhong ChuanhongYe LuLiu JinsongRen TianjianMa Weichao