STAT3
- Known as:
- STAT3
- Catalog number:
- RP17131630010
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- STAT3
Related genes to: STAT3
- 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
Acpin1,Acrosomal protein ACPIN1,Mouse,Mus musculus,Sipar,STAT3-interacting protein as a repressorAnserine Signal Transducer And Activator Of Transcription 3 Elisa Kit (STAT3)Anserine anti - Signal Transducer And Activator Of Transcription 3 Elisa Kit (STAT3)Anti- STAT3 (Ab-705) AntibodyAnti- STAT3 (Ab-705) AntibodyAnti- STAT3 (Ab-727) AntibodyAnti- STAT3 (Ab-727) AntibodyAnti- STAT3 (Phospho-Ser727) AntibodyAnti- STAT3 (Phospho-Ser727) AntibodyAnti- STAT3 (Phospho-Tyr705) AntibodyAnti- STAT3 (Phospho-Tyr705) AntibodyAnti-Human STAT3, Rabbit PolyclonalAnti-Human STAT3, Rabbit Polyclonal affinity purified IgGanti-n STAT3 , Rabbit polyclonal to n STAT3 , Isotype IgG, Host RabbitAnti-phospho-STAT3 (pTyr705<_SUP>) produced in rabbit Antibody Related articles to: STAT3
- Metastasis and chemoresistance are the leading causes of death in high-grade serous ovarian carcinoma (HGSOC). Our previous studies revealed that the membrane protein cytochrome b reductase 1 (CYBRD1) is a critical prognostic marker for HGSOC, but its role in HGSOC progression and molecular mechanisms remain unclear. Here, we reveal that CYBRD1 is a druggable factor that drives chemoresistance and tumor progression in HGSOC. Importantly, compared with that in their cisplatin-sensitive counterparts, CYBRD1 expression is elevated in cisplatin-resistant cells. Through genetic manipulation, we showed that CYBRD1 inhibition effectively re‑sensitizes cells to cisplatin and suppresses proliferation, migration, and invasion. Targeted gene expression profiling indicated that CYBRD1 inhibition markedly attenuated JAK2/STAT3 signaling. Using point mutants, we confirmed that phosphorylation of CYBRD1 at Tyr252 is essential for the interaction with JAK2, subsequent activation of JAK2/STAT3 signaling and mediating HGSOC progression. CYBRD1 inhibition significantly restored cisplatin sensitivity and exerted a synergistic tumoricidal effect. In vivo, combined CYBRD1 inhibition and cisplatin markedly reduced tumor metastasis. Furthermore, we found that RUNX1 regulates CYBRD1 transcription. These findings highlight that the combination of CYBRD1 inhibitors and conventional chemotherapy is a promising therapeutic strategy for HGSOC, especially in chemoresistant patients. - Source: PubMed
Publication date: 2026/07/29
Deng YalongGan QiyuHuang XiaZhu LiangLiu LinaWang GuozengChang LinlinShi RuiQiang SufengDuan WenzhiLiu QinLei HuiMinCheng Jingxin - Glioblastoma (GBM) is the most aggressive primary brain malignancy, with a median survival of approximately 15 months despite current standard-of-care treatment. N6-methyladenosine (m6A) RNA modification regulates gene expression, but its relationship with miRNA-mediated regulation, metabolism, and prognosis in GBM remains incompletely understood. We hypothesized that integrating m6A regulators, miRNA-mRNA interactions, and clinical data could identify molecular relationships associated with GBM prognosis. We analyzed RNA-seq, miRNA expression, and clinical data from 160 matched TCGA-GBM patients using survival-based differential expression, Pearson correlation, network analysis, and Cytoscape visualization. A ten-gene Cox regression prognostic signature was developed and evaluated using Kaplan-Meier and time-dependent ROC analyses and externally validated using GSE83300. Functional enrichment and Hallmark Gene Set Enrichment Analysis (GSEA) were performed to characterize associated biological pathways. We identified 173 survival-associated mRNAs and 87 miRNAs, with 682 significant m6A-mRNA associations and 151 negatively correlated miRNA-mRNA pairs forming a network of 833 edges across 189 nodes. ALKBH5, WTAP, and YTHDF1 emerged as highly connected transcriptomic hubs. The ten-gene signature was significantly associated with overall survival (HR = 2.55, 95% CI = 1.85-3.53; p = 1.39 × 10; 1-year AUC = 0.768) and was externally validated (AUC = 0.719). Strong gene-level associations were observed between m6A regulators and metabolism-related genes, including WTAP-LDHA (r = 0.56) and FTO-ACACA (r = 0.75). GSEA identified significant enrichment of EMT (Epithelial-Mesenchymal Transition), TNF-α/NF-κB, IL-6/JAK/STAT3, angiogenesis, and hypoxia pathways, whereas glycolysis showed a non-significant enrichment trend (FDR = 0.294). Overall, these findings link m6A-associated transcriptional networks with metabolic and inflammatory features and prognostic variation in GBM, providing a hypothesis-generating framework for further experimental investigation. - Source: PubMed
Publication date: 2026/10/07
Rana Md SohelParvin Mst MoriumSarker Md AshrafulIslam Md TariqulRahman Md MatiurWahid Abdul - The efficacy of immunotherapy in nasopharyngeal carcinoma (NPC) is limited by heterogeneous mechanisms of immune evasion. Identifying robust molecular biomarkers that predict this phenotype is crucial for patient stratification. This study aimed to identify candidate genes derived from a predefined methylation-related gene set and to evaluate their association with tumor-immune features in NPC using an integrative computational and experimental approach. - Source: PubMed
Publication date: 2026/09/26
Li MengchengYi AnJiang Chunling - Hand-foot syndrome (HFS) is a frequent and potentially dose-limiting adverse event of capecitabine. Current therapeutic strategies are not always effective. Since inflammatory pathways, including JAK-STAT3 signaling, may contribute to capecitabine-induced HFS, topical JAK inhibition could represent a potential therapeutic approach. - Source: PubMed
Publication date: 2026/10/07
Rapparini LucaMartelli GinevraCedirian StephanoPampaloni FrancescaBruni FrancescaStarace Michela - To investigate the protective effects of kaempferol (KPF) against gestational diabetes mellitus (GDM) and elucidate its underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/09/22
Liu RonghuiLiu QiqiYi Lanjie