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
- Metastatic breast cancer remains a major therapeutic challenge due to the limited efficacy of current treatments against both primary tumors and distant metastases. Here, we developed an arginine-based click-crosslinked nanoplatform for the co-delivery of camptothecin (CPT) and STAT3 siRNA (siSTAT3). The nanoplatform was constructed using a dibenzocyclooctyne-functionalized arginine derivative, where guanidinium-phosphate interactions enabled efficient siRNA loading and copper-free click crosslinking improved structural stability. Hyaluronic acid modification further enhanced tumor cell uptake through CD44 recognition. HDCPT@siSTAT3 achieved efficient intracellular delivery, lysosomal escape, and intracellular release of CPT and siSTAT3. In 4T1 breast cancer cells, HDCPT@siSTAT3 reduced STAT3 expression by approximately 50%, promoted apoptosis, and inhibited migration. In 4T1 breast tumor models, HDCPT@siSTAT3 suppressed tumor growth with minimal systemic toxicity. Moreover, the treatment significantly decreased lung metastatic burden in a 4T1-Luc metastasis model. The integration of arginine-based interactions, covalent cross-linking, and active targeting may provide a useful strategy for combined chemo-gene therapy in metastatic breast cancer. - Source: PubMed
Publication date: 2026/09/04
Xiong SuXiang JinghengHe XiaoGan ChunyuanLiu YuGuo XiaoLi DaxiuXie Jing - This correspondence provides a critical perspective on the recent study by Zhao et al. defining the hyperglycemia-STAT3-neutrophil extracellular trap-thromboinflammation axis in post-ischemic stroke hemorrhagic transformation. Beyond three core unresolved scientific gaps concerning cell-type specificity, tissue plasminogen activator-associated pathological context, and glycemic model heterogeneity, we extend the discussion to supplementary translational constraints, the upstream regulatory role of mitochondrial oxidative stress, and implications for clinical trial design. These viewpoints aim to further enhance the translational potential of this promising therapeutic target. - Source: PubMed
Publication date: 2026/09/04
Yang Yuan - A formal synthesis of cortistatin A, a marine-derived steroidal alkaloid with potent anti-angiogenic and antileukemic activities, was achieved via a unique synthetic strategy that leveraged a late-stage SmI-mediated oxa-bridge translocation. The de novo-synthesized simplified analog CA411 was evaluated across 38 cell lines, revealing potent and selective antiproliferative activity against a diffuse large B cell lymphoma (DLBCL) line OCI-Ly3. Time-course transcriptomics and mechanistic studies demonstrated that it disrupts an autocrine IL-6-JAK2-STAT3 signaling loop, reducing IL-6 secretion, STAT3 phosphorylation, and downstream anti-apoptotic genes, thereby inducing apoptosis. Not only this selectivity extends to other CDK8/19 inhibitors and IL-6-dependent models, but CA411 also suppressed OCI-Ly3 xenograft growth, diminished IL-6 expression, induced anti-angiogenic effects with vascular normalization, and prolonged survival in mouse models. These findings position CDK8/19 inhibitors like cortistatins as leads for IL-6-dependent lymphomas, highlighting a targetable vulnerability in cytokine-driven malignancies and bridging synthetic innovation with therapeutic discovery. - Source: PubMed
Publication date: 2026/09/04
Wang WenjunZhang NanChen BaichengChen ZijingZeng GuihuaLuo Tuoping - Sevoflurane (SEV) is widely used in clinical anesthesia, but its exposure is increasingly being linked to neurocognitive dysfunction, particularly in hippocampal neurons. TRIM14, an E3 ubiquitin ligase, is essential for regulating inflammation, apoptosis, and mitochondrial function; however, its involvement in SEV-induced neuronal damage remains unclear. In this study, we investigated the role of TRIM14 in SEV-induced hippocampal neuronal damage, focusing on mitochondrial dysfunction, iron homeostasis, and inflammation. The results show that TRIM14 knockdown significantly increased cell viability, restrained apoptosis, and suppressed inflammatory cytokines in SEV-treated neurons. However, it also alleviated mitochondrial dysfunction, mitigated ferroptosis, and regulated iron homeostasis. Furthermore, silencing TRIM14 suppressed the NF-κB and STAT3 axis. These findings suggest that TRIM14 contributes to SEV-induced neuronal damage. - Source: PubMed
Publication date: 2026/09/04
Wang ChunYan EnjunQu Dongchao - Breast cancer (BC) is the second most prevalent malignancy after lung cancer, and the life expectancy is still very low due to therapeutic resistance and tumor relapse. It is crucial to identify novel biomarkers that can serve as potential therapeutic targets. In TNBC, aberrant activation of EGFR has also been implicated in the development of drug resistance. STK35L1 is a critical regulator of diverse cellular processes, including apoptosis and DNA damage. Notably, STK35L1 promotes drug resistance and regulates glycolysis and apoptosis through AKT signaling. The oncogenic role of STK35L1 is established in various cancers, including osteosarcoma, colorectal cancer, and acute myeloid leukemia. However, its association in BC has not yet been explored. In this study, we found that STK35L1 was significantly upregulated in multiple cancers, and its higher expression was associated with poor survival outcomes in BC patients. STK35L1 was differentially upregulated across all BC subtypes. An association between EGFR and STK35L1 expression was observed in normal breast tissues but not in BC. Interestingly, compared with normal breast tissue, EGFR mRNA expression is downregulated in BC tissues, with the greatest downregulation in the luminal B subtype and the least in TNBC. Furthermore, EGFR inhibition with gefitinib increased STAT3 phosphorylation at Tyr-705, and STK35L1 and EGFR gene expression were significantly upregulated. These data suggest that EGFR-STAT3 signaling may regulate STK35L1 and EGFR expression. In conclusion, we report an association of STK35L1 and EGFR in BC, highlighting STK35L1 as a potential prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/09/04
Bage SaloniYadav ArpanaGaur KritikaGahlot KritikaPurva MukulSaini MaheshDadarwal SunitaGehlot PragyaKumari SudhanshuBhutra ShyamSawant Devesh MadhukarBrünnert DanielaKasliwal NeenaGoyal Pankaj