Stat3 (phospho-Tyr705) Antibody
- Known as:
- Stat3 (phosphorilated-Tyr705) Antibody
- Catalog number:
- abx000144
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- 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
- Patients with advanced high-grade serous ovarian carcinoma (HGSOC) often experience extremely poor prognoses due to extensive peritoneal metastases, yet the underlying driving mechanisms remain unclear. This study reveals that serum amyloid A1 (SAA1) is markedly upregulated in late-stage HGSOC and is closely associated with poor prognosis and distant metastasis. These findings were validated through both single-cell RNA sequencing and clinical specimen analyses. Surprisingly, SAA1 does not directly promote tumour cell proliferation or migration. Instead, it reshapes the immunosuppressive tumour microenvironment by activating FPR2 tumour-associated macrophages (TAMs). Mechanistically, the SAA1-FPR2 signalling axis triggers the JAK2/STAT3 pathway in macrophages, enhancing the transcription and secretion of CXCL1. This, in turn, induces epithelial-mesenchymal transition (EMT) in tumour cells and endows them with greater metastatic potential. Animal models further confirmed that SAA1 knockdown, macrophage depletion, or CXCL1 blockade all significantly suppressed peritoneal dissemination. Collectively, this study identifies a novel SAA1-TAM-CXCL1 immune-inflammatory signalling axis, elucidates its critical role in ovarian cancer metastasis, and provides a robust theoretical foundation for the development of innovative anti-metastatic therapeutic strategies. KEY POINTS: A distinct SAA1-enriched tumour cell subset with metastasis-associated features is identified in ovarian cancer. Tumour-derived SAA1 reprograms TAM through FPR2-mediated JAK2-STAT3 signalling to induce an immunosuppressive phenotype. The SAA1-TAM-CXCL1 axis facilitates metastatic progression in ovarian cancer. - Source: PubMed
Zhou XuanMeng HuangyangChang QianjingRen JingjingWen MeichenZhang LinCheng Wenjun - Lung cancer remains the leading cause of cancer-related mortality, with poor outcomes driven by late presentation and therapy resistance. Although genes encoding secreted proteins may reflect tumor biology and have biomarker potential, systematic multi-cohort studies identifying and validating prognostically relevant secreted-protein candidates in non-small cell lung cancer (NSCLC) are limited. - Source: PubMed
Publication date: 2026/05/18
Kim JoonLee GeuninYong Seung-HyunKim Eun YoungJo YunjuJeong WoojuRyu DongryeolOh Chang-MyungLee Sang Hoon - Neuroinflammation following spinal cord injury (SCI) is primarily driven by abnormal microglial activation and represents a major barrier to neurological recovery. This study aimed to investigate the regulatory role of leptin (LEP) in SCI, with a particular focus on its effects on the JAK-STAT signaling pathway, microglial polarization, and neuronal injury. Transcriptome sequencing of spinal cord tissues was performed to identify differentially expressed genes (DEGs), followed by enrichment, immune cell infiltration, and protein-protein interaction (PPI) analyses to determine key pathways involved in SCI. A mouse SCI model was established, and LEP expression was silenced using shRNA. Motor function recovery and pathological changes were assessed by Basso-Beattie-Bresnahan scoring, rotarod testing, Nissl staining, and hematoxylin-eosin staining. qRT-PCR, Western blot, and immunofluorescence were used to examine inflammatory mediators, microglial polarization markers, and JAK-STAT signaling. LPS-stimulated BV2 and primary microglia were used to evaluate the effects of LEP on inflammatory activation and polarization, and interferon gamma (IFN-γ) was applied to verify the involvement of JAK-STAT signaling. A microglia-PC12 co-culture system was used to determine the effects of LEP intervention on neuronal apoptosis and oxidative stress. Transcriptomic profiling revealed a marked enhancement of inflammation- and immunity-related pathways after SCI, with the JAK-STAT pathway identified as a major regulatory axis strongly associated with upregulated LEP expression. Functional analyses showed that LEP knockdown significantly improved motor recovery after SCI. LEP silencing suppressed the phosphorylation of JAK2 and STAT3, promoted the shift of microglia from the M1 to the M2 phenotype, reduced iNOS, TNF-α, and IL-6, and increased IL-4 and IL-10 expression. IFN-γ partially reversed these effects, confirming that LEP regulates microglial polarization through the JAK-STAT pathway. LEP knockdown in microglia also attenuated neuronal apoptosis and oxidative stress, decreasing cleaved caspase-3, Bax, MDA, and ROS levels while restoring Bcl-2 and enhancing SOD activity. LEP may function as a modulator associated with JAK-STAT signaling activation during neuroinflammation after SCI. Integrating transcriptomic and mechanistic evidence, we demonstrate that LEP silencing is associated with suppressed activation of JAK-STAT pathway, promotes M2 microglial polarization, reduces neuronal apoptosis and oxidative damage, and ultimately enhances spinal cord repair and functional recovery. - Source: PubMed
Publication date: 2026/05/17
Chen ChunTian XiaoweiZhang WenyanWang XianjinZhao LinfengMa YucangZhang ChenhongHuang HaoTang WeiweiZhu XiaoshengBai ZhaoqingDing Fusheng - Yiqi Huoxue Lishui (tonifying qi, promoting blood circulation, and promoting diuresis to relieve water retention) is a core therapeutic principle in traditional Chinese medicine for the treatment of post-myocardial infarction heart failure (PMI-HF). Optimized New Shengmai Powder (ONSMP) is a traditional prescription composed of Astragalus mongholicus (Huangqi), Codonopsis pilosula (Dangshen) and other Chinese medicinal herbs. It has long been used in northern China to treat cardiovascular diseases such as "chest impediment" and heart failure characterized by qi deficiency, blood stasis and water retention according to traditional Chinese medicine theory. Clinical practice suggests that ONSMP can improve symptoms and cardiac function in such patients, but the modern pharmacological basis of its cardioprotective effects remains unclear. In recent years, ferroptosis-related oxidative injury has been recognized as a key mechanism driving the progression of PMI-HF. Whether ONSMP regulates this pathological process, and through which molecular pathways, remains to be elucidated. - Source: PubMed
Publication date: 2026/05/16
Zhang ZeyuYang ZhihuaWang CiSong YuweiGuo LiuliWang ShuaiWang XianliangMao Jingyuan - High-mobility group box 1 (HMGB1), a protein with context-dependent pro- and anti-tumor functions, is expressed in tumor cells, tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), cancer-associated fibroblasts, and T cells within the tumor microenvironment (TME). The identity of HMGB1 has undergone a transformation from a nuclear architectural protein to a secreted damage-associated molecular pattern (DAMP) with pivotal roles in inflammation and cancer. The heterogeneity of HMGB1 stems from the diversity of post-translational modifications, proteolytic cleavage and lysis, partial independence of domain functions, differences in source tissues and cells, concentration-dependent effects, spatiotemporal distribution and dynamics, and functional diversity. This review summarizes the roles and molecular mechanisms of nuclear, cytoplasmic, and extracellular HMGB1 derived from different cells in tumor progression, its targeted therapy, and its application value as a biomarker, highlighting the regulation of HMGB1 and the downstream signaling pathways of HMGB1. HMGB1 mainly exerts pro-tumor effects during tumor progression via multiple downstream pathways (MAPK, NF-κB, PI3K/AKT, Wnt, STAT3, etc.), while its subtle induction of cell death and enhancement of the immune response demonstrate moderate anti-tumor effects. HMGB1-mediated immune crosstalk regulates the proliferation, growth, migration, invasion, and chemoresistance of tumors. A comprehensive investigation of the spatiotemporal dynamics of HMGB1 and its underlying molecular regulatory mechanisms using cutting-edge technologies, including single-cell RNA sequencing, spatial transcriptomics, and real-time live-cell imaging, will facilitate the development of precise, mechanism-informed therapeutic interventions. Given the multifaceted challenges posed by tumor heterogeneity, the dual pro- and anti-tumor functions of HMGB1, and the limitations of targeting technologies, HMGB1-targeted strategies hold substantial promise for clinical translation. - Source: PubMed
Publication date: 2026/05/16
Chu JueqiongDong ChunlingLi Bo