STAT3 (Phospho_Ser727) Antibody
- Known as:
- STAT3 (Phospho_Ser727) Antibody
- Catalog number:
- E011046-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- STAT3 (Phospho_Ser727) Antibody
Related genes to: STAT3 (Phospho_Ser727) 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_Ser727) Antibody
Related articles to: STAT3 (Phospho_Ser727) Antibody
- Lung cancer is the most common pulmonary malignancy. WHO data show that its incidence and mortality are rising globally, severely threatening public health. - Source: PubMed
Sun JiaJifu CiliQiu YanliLu LinxiaXu ZhenyuHe ZilinWang Jingtao - SHMT2 (serine hydroxymethyltransferase 2) is a pivotal enzyme in cellular metabolism and is closely associated with the initiation and progression of malignant tumors, garnering significant attention in cancer research and therapy. Aberrant expression of SHMT2 has been observed in various cancers, correlating with tumor aggressiveness and patient prognosis. Functionally, SHMT2 participates in one-carbon metabolism, supplying methyl donors and biosynthetic precursors to support tumor cell proliferation. Additionally, it modulates redox homeostasis, promoting cancer cell survival and progression. SHMT2 also interacts with key signaling pathways, including JAK2/STAT3 and Akt/mTOR, thereby influencing tumor cell growth, invasion, and metastasis. Further elucidation of the molecular mechanisms by which SHMT2 contributes to tumorigenesis may provide critical insights for precision diagnosis, targeted therapy, and prognostic evaluationin oncology. - Source: PubMed
Publication date: 2026/08/18
Li MeiXu Ya NanSu XiulanWen Jianxun - Atopic dermatitis (AD) is a prevalent chronic skin disease worldwide. Emerging evidence suggests that an elevated salt microenvironment is a unique characteristic of skin lesions in AD patients. Emerging data indicate that lesional skin in AD contains abnormally high salt, yet how this microenvironment affects keratinocytes is unknown. We interrogated the impact of elevated NaCl on barrier function and inflammation using HaCaT cells , and 2,4-dinitrofluorobenzene (DNFB) and ovalbumin (OVA) treatment induced an AD model of mice . The interaction between SGK-1, mTOR, STAT3, and NFκB was identified with their roles in AD, analyzed through loss-of-function assays and pharmacological inhibitions. Our results showed that the high-salt microenvironment impaired keratinocyte differentiation and promoted inflammatory cytokine production, thereby exacerbating the disease. Mechanistically, NaCl activated STAT3 via the SGK-1-mTOR signaling pathway in keratinocytes, leading to a decrease in the expression of epidermal barrier proteins. In addition, inflammatory cytokines were increased by NaCl-induced SGK-1-mTOR-NFκB activation. We identified the SGK-1 inhibitor GSK 650394, which could rescue the NaCl-induced blockade of keratinocyte differentiation and inflammatory cytokine production. Moreover, in combination with the JAK inhibitor delgocitinib, GSK 650394 exhibits a synergistic effect in ameliorating AD-like symptoms . Taken together, our findings demonstrate that the high-salt microenvironment promotes the development of AD by activating the SGK-1-mTOR pathway in keratinocytes, suggesting that an SGK-1 inhibitor could potentially serve as a drug to alleviate AD-like symptoms. - Source: PubMed
Publication date: 2026/03/27
Luo YingqiangSong ZhiqiangJiang PengjuGe LanZhang MinZhou ZihaoWu YaguangHu Jun - AD is a neurodegenerative disorder marked by progressive cognitive decline, particularly memory impairment, largely driven by cholinergic dysfunction. This study aimed to investigate the pharmacological basis and modes of action of the identified TT-TeMac™ compounds againsts cholinergic dysfunction associated with memory loss. TT-TeMac™ compounds targets which were identified by LC-MS were extracted from SwissTarget Prediction and PharmMapper, while cholinergic dysfunction-related targets were obtained from DisGeNET and GeneCards. Fifteen common targets were identified, with nine key targets highlighted by STRING, Cytoscape, and Venny analyses and confirmed by molecular docking using MOE. The validation used a rat model with scopolamine-induced cholinergic dysfunction (1 mg/kg bw/day, ip) for 7 days. Subsequently, behavioral (NOR and MWM), biochemical (AchE and BuhE) and histological (H&E and CV) analyses were performed. Seven compounds were identified in TT-TeMac™ (terminolic acid, sericic acid, arjunolic acid, gallic acid, ellagic acid, 3-O-methyl ellagic acid and 3,3'-di-O-methyl ellagic acid). Network pharmacological analysis showed that TT-TeMac™ acted on 15 common targets of which ACHE, IL6, TNF, SNCA, AKT1, SERPINE1, STAT3, ACE, and ALB were the pivotal genes. Also, docking studies confirmed the involvement of the target within the network with meaningful binding energies. Furthermore, TT-TeMac™ prevented cholinergic dysfunction associated with memory loss in rats by significantly reducing cholinesterase activity and protecting against morphological alterations and neuronal loss in the hippocampus. Our study shows that the ingredient TT-TeMac™ has a multi-targeted mode of action on protein targets involved in cholinergic dysfunction and counteracts this dysfunction in scopolamine-treated rats. - Source: PubMed
Publication date: 2026/08/10
Ambamba Bruno Dupon AkambaJonathan Messanga Me Ngo'oMarc Akono Fama YvesSandrine Nyabissick MondjiepReine Njayou Mbouangouore IngridEmmanuel NgarchindiLaurent Nkodo AbegaBlonde Njanjo Ejanmoua Merveille LaAlexandra Ebogo Enyegue FrançoiseElla Fils ArmandMandob Damaris EnyegueNgondi Judith Laure - Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with disrupted iron homeostasis, lipid peroxidation, and ferroptosis-related liver injury. Although exercise is recommended for MASLD management, whether moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) exert comparable effects on hepatic iron metabolism and ferroptosis-related changes remains unclear. This study compared the effects of MICT and HIIT on hepatic iron homeostasis, ferroptosis-related markers, and lipid metabolic remodeling in high-fat diet (HFD)-induced MASLD rats. Forty male Sprague-Dawley rats were assigned to a normal-fat diet group or an HFD group. After 8 weeks of HFD feeding, HFD-fed rats were further divided into HFD control, MICT, and HIIT groups and underwent an additional 8-week intervention. HFD feeding induced metabolic dysfunction, hepatic steatosis, liver injury, iron accumulation, increased activation-related markers of the IL-6/JAK2/STAT3-hepcidin pathway, and ferroptosis-related changes, including reduced GPX4 and increased PTGS2 and MDA. Both MICT and HIIT improved metabolic and histological outcomes, reduced hepatic Fe accumulation and lipid peroxidation, increased FPN1 expression, decreased DMT1 expression, reduced activation-related markers of IL-6/JAK2/STAT3-hepcidin signaling, and improved antioxidant defense. Untargeted lipidomics indicated partial remodeling of HFD-induced disturbances in glycerophospholipid, glycerolipid, sphingolipid, ether lipid, thermogenesis, insulin-resistance, and AMPK-related pathways. Most endpoint outcomes did not differ significantly between MICT and HIIT. Because no pathway-specific manipulation, iron-rescue experiment, or ferroptosis inhibitor was used, the present data do not establish that the IL-6/JAK2/STAT3-hepcidin-FPN1 axis causally mediates the exercise response. Instead, the findings indicate that MICT and HIIT exert broadly comparable protective effects that are associated with improved hepatic iron homeostasis, lower ferroptosis-related susceptibility, and hepatic lipid metabolic remodeling. - Source: PubMed
Publication date: 2026/08/20
Wang ShijieLi ChangLiu YufeiXu Lin