Ask about this productRelated genes to: STAT3 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 antibody
Related articles to: STAT3 antibody
- DRP1 (dynamin-related protein 1) mediates mitochondrial fission and permits rapid cell cycle progression in hyperproliferative cells by coordinating nuclear and mitochondrial division, a process called mitotic fission. However, DRP1 alone appears insufficient to complete fission, and the link between fission and cell cycle progression is unknown. We hypothesize that DNM2 (dynamin 2) interacts with DRP1 to complete mitochondrial fission and regulate cell cycle progression. We show that DNM2 is upregulated in pulmonary artery smooth muscle cells (PASMCs) in human and rodent pulmonary arterial hypertension (PAH) PASMCs, contributing to disease pathophysiology. - Source: PubMed
Publication date: 2026/04/28
Dasgupta AsishChen Kuang-HueihWu DanchenYerramilli V SiddarthaLima Patricia D AMartin Ashley YBentley Rachel E TOtt Benjamin PNandani TanviMewburn Jeffrey DTian LianAl-Qazazi RuaaEmon Isaac MColpman PierceJefferson LindsayNoordhof CurtisJones OliverHindmarch Charles C TArcher Stephen L - Squamous cell carcinomas (SCCs) originate in epithelial tissues of older individuals who have been exposed to environmental carcinogens. Despite overlapping clinical hallmarks, SCCs from different anatomic sites have different prognoses. Here we show that fibroblasts confer site-specific cues that determine SCC proliferation and invasion. Oral and lung fibroblasts have distinct lipid metabolism, transferring unique lipids to SCC cells that promote epithelial-to-mesenchymal transition, and oral and lung SCC invasion. Whereas oral fibroblasts transfer sphingomyelins, which activate the ceramide-sphingosine-1-phosphate-STAT3 pathway and promote oral SCC invasion, lung fibroblasts transfer triglycerides to lung SCCs, thereby triggering cholesterol synthesis and invasion, which is associated with poor survival. By contrast, dermal fibroblasts are lipid poor, and cutaneous SCC is less invasive. Our data indicate that targeting fibroblast lipid synthesis and SCC lipid uptake or breakdown inhibits oral and lung epithelial cancer invasion. - Source: PubMed
Publication date: 2026/04/27
Budden TimothyPalombo NoahGurung ShilpaGutteridge MarthaRussell CharlotteMarques Jairvon Kriegsheim AlexAn LyutongHarwood CatherineMotta LuisaJorgensen ClausLópez-Garcîa CarlosGaudy-Marqueste CarolineHarrington KevinPedersen MalinO'Leary BenRullan AntonioVirós Amaya - Itaconate is a Krebs cycle-derived metabolite with anti-inflammatory and antiviral properties. This particularly applies to derivatives of itaconate, notably 4-octyl itaconate (4-OI), which has been extensively studied in models of inflammation and infection. Itaconate and 4-OI have been shown to exhibit antiviral activity against Zika virus, Influenza A virus (IAV) and Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2). Here we have further analysed the effect of itaconate and 4-OI on SARS-CoV-2 infection. 4-OI inhibited replication of SARS-CoV-2 in vitro and in vivo, in agreement with recent literature. In lung epithelial cells, 4-OI potently blocked expression of the SARS-CoV-2 uptake receptor, Angiotensin-converting enzyme 2 (ACE2), reducing ACE2 dependent uptake of viral pseudo particles. 4-OI inhibited the induction of both a truncated version of ACE2 and signal transducer and activator of transcription 3 (STAT3)-dependent full-length ACE2, possibly because of its inhibitory effect on Janus kinase 1 (JAK1). Inhibition of JAK1 by 4-OI will therefore block ACE2 expression as well as other effects driven by JAK1, highlighting a dual capability of itaconate derivatives such as 4-OI for having antiviral and anti-inflammatory effects, which could have therapeutic utility in COVID-19. - Source: PubMed
Publication date: 2026/04/25
Weiss Hauke JHooftman AlexanderSalgado-Benvindo ClarisseBoudewijns RobbertLiesenborghs LaurensRyan Tristram A Jvan der Horst DemiCarter-Timofte Madalina EGewaid HossamBowie AndrewThibaut Hendrik JanDallmeier KaiOlagnier Davidvan Hemert Martijn JO'Neill Luke A J - Acute pancreatitis (AP) is an acute inflammatory abdominal disease frequently associated with intestinal barrier dysfunction. The steroid hormone 17β-estradiol is an estrogen that exhibits anti-inflammatory effects in various inflammatory diseases. However, its potential beneficial effects on AP and the underlying mechanism have not been investigated. - Source: PubMed
Publication date: 2026/04/20
Shan WeixiZhou WenyuHuang YaOu HengyangYang Long - Butein, a naturally occurring chalcone, exhibits diverse pharmacological potential but suffers from limited anticancer efficacy. To address this limitation and improve drug-likeness, we designed and synthesized a novel series of 3-deoxy-4-sulfonamido-butein derivatives. The synthesized compounds were evaluated for their antiproliferative activities against human non-small cell lung cancer (NSCLC) cells, including A549, H1299, and H1975 lines. Among them, compounds 8o (MRC-B-016) and 8p (MRC-B-018), characterized by electron-donating dialkylamino substituents, demonstrated profoundly enhanced growth inhibition compared to the parent compound without significant cytotoxicity in WI-38 normal lung cells. Mechanistic investigations revealed that 8o (MRC-B-016) and 8p (MRC-B-018) effectively induced G2/M cell cycle arrest and apoptotic cell death. Furthermore, these lead candidates operated through a convergent dual-targeting mechanism by directly inhibiting epidermal growth factor receptor (EGFR) tyrosine kinase activity while concurrently suppressing the downstream JAK2/STAT3 signaling axis. Molecular docking simulations corroborated these biological outcomes, displaying highly favorable binding interactions within both the EGFR kinase and STAT3 SH2 domains. Notably, these derivatives successfully suppressed oncogenic activation and colony formation even in gefitinib-resistant NSCLC models. Collectively, this study identifies sulfonamide-modified butein derivatives, particularly 8o (MRC-B-016) and 8p (MRC-B-018), as promising dual-targeting agents. Future research will focus on expanding the structure-activity relationship and conducting comprehensive in vivo evaluations to advance these chemotypes toward clinical translation for treatment-resistant lung cancer. - Source: PubMed
Publication date: 2026/04/22
Choi Jung HwanHwang Hyun-HaHong JinwonKim Jeong UkRoh Geon WanCho YewonByun JoonseokJe Jeong-HuiLee Hyeong-ChanYoo Ji-SungLee SangjunHa JinSeokKim Tae-HyounKo Seong-GyuLee Jae Yeol