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
- In this work, we developed bispecific antibody (bsAb)-derived surrogate agonists which mimic the function of IL-21 by targeting the IL-21 receptor composed of IL-21 R (CD360) and IL-2 Rγ (CD132). For this, antigen-specific VHHs (variable domains of the heavy chain of heavy-chain-only antibodies) were obtained by immunization of camelids and isolated using yeast surface display. Combinatorial reformatting of IL-21 R-specific single‑domain antibodies (sdAbs) and IL-2 Rγ-targeting paratopes into a monovalent bispecific antibody architecture enabled the identification of IL-21 mimetics displaying attenuated capacities in triggering STAT3 phosphorylation compared to the wild-type cytokine as demonstrated in NK-92 cells as well as peripheral blood mononuclear cells (PBMCs). Moreover, by applying different protein engineering strategies, we demonstrate that agonism capacities of the generated IL-21 mimetics, such as pSTAT3 induction or Granzyme B expression of cytotoxic T cells, can be significantly optimized. For this, framework mutations were introduced to engineer VHH:VHH interactions within the bispecific sdAb-Fc fusion geometry for a more rigid receptor targeting. Furthermore, we show that antibody format engineering, in which the VHHs were arranged in an IgG-like scaffold that replaces the conventional IgG VH and VL domains with the corresponding VHHs, combined with rigidifying mutations, enables IL-21 R agonism comparable to the wild-type cytokine. Taken together, these findings show that IL-21 receptor agonism can be substantially optimized by adapting the spatial orientation of paratopes targeting both receptor subunits via forced dimerization, without altering paratope valencies. - Source: PubMed
Publication date: 2026/09/02
Lipinski BrittaUnmuth LauraTran Thi Hong HueHarwood JakobArras PaulBecker StefanHarwardt JuliaGuarnera EnricoHelming LauraZaynagetdinov RinatBertoldo DavideRajpal ArvindElter DesislavaPekar LukasEvers AndreasZielonka Stefan - The prevalence of food allergy has been rising over the past decade, but effective treatments remain limited. The purpose of this study was to investigate the effect of ginkgolide B (GB), a natural bioactive compound with well-documented anti-inflammatory and immunoregulatory properties, on a mouse model of food allergy and to elucidate the mechanism mediated by the mTOR signaling pathway. - Source: PubMed
Publication date: 2026/08/18
Zhou RongqinYang XiaotongTan PanpanWang HuanZeng DanMa Xiaojuan - Blood-brain barrier (BBB) disruption is a hallmark of acute traumatic brain injury (TBI), yet the immune-vascular mechanisms underlying endothelial dysfunction remain incompletely understood. Perivascular macrophages (PVMs) are strategically positioned to modulate cerebrovascular homeostasis, but their role in acute post-traumatic endothelial activation has not been systematically characterized. - Source: PubMed
Publication date: 2026/08/18
Lin YanyaLin ChengdaChen JianhuiChen ShijunHuang JianhuangHu Jianxiong - This study aims to analyze the expression of miR-324-3p in acute myocardial infarction (AMI), as well as its regulatory effects on inflammatory responses, oxidative stress, and cell viability in cardiomyocytes. - Source: PubMed
Publication date: 2026/07/25
Liu HongxiaZhu WenjingWang WenzhengTang Ruishuang - The presence of thin endometrium (TE) and defective embryo implantation, indicative of endometrial disorders, majorly contributes to sterility. The Sun's Bushen Huayu formula (BHD), a multi-herbal decoction prepared under standardized conditions, has shown potential in modulating M1/M2-associated inflammatory markers, but its efficacy in endometrial repair remains unclear. Female Sprague-Dawley rats with confirmed regular estrous cycles were first subjected to a thin endometrium (TE) model induced by hydroxyurea, high-molecular dextran, and intrauterine ethanol injury. After model establishment, rats received oral BHD or vehicle for 20 days, then were mated. On gestational day 8, uterine tissues were collected for analysis. Estrous cycle synchronization, body weight dynamics, embryo count, and histopathological evaluation were performed. Immunohistochemistry for M1/M2 macrophage markers, cytokine profiling by ELISA, and molecular analyses (qRT-PCR, flow cytometry) of M1/M2-associated markers and endometrial repair markers were conducted. In addition, western blotting was performed to examine STAT3 activation, apoptosis-related proteins, and nuclear/cytoplasmic NF-κB signaling. The administration of BHD notably lessened body weight loss and improved reproductive outcomes, as indicated by increased embryo implantation compared with the Model group, although implantation was not fully restored to Control levels. Representative histological analysis showed that BHD improved endometrial morphology. Treatment with BHD altered the expression of M1- and M2-associated markers, as evidenced by elevation of Arg-1 (an M2-related marker) and reduction of iNOS (an M1-related marker) in uterine tissue. Mechanistically, BHD was associated with a reduced p-STAT3/STAT3 ratio, decreased Cleaved-Caspase-3 and Bax expression, restored Bcl-2 levels, lower nuclear p-NF-κB/NF-κB, and higher cytoplasmic p-NF-κB/NF-κB, suggesting attenuation of inflammatory-apoptotic signaling and a shift in NF-κB subcellular distribution. Molecular analyses confirmed BHD's role in shifting the balance of M1/M2-associated markers, increasing CD206 cell populations, and reducing CD86 cells in uterine tissue. BHD was associated with improved endometrial repair in a TE model, accompanied by changes in M1/M2-related markers and cytokine balance. These findings suggest that BHD may serve as a potential therapeutic agent for restoring endometrial function and enhancing reproductive outcomes in conditions associated with endometrial dysfunction. - Source: PubMed
Publication date: 2026/08/17
Liao YanfengZhang HongqingLian FeiyanChen LihuiHuang Shaoqun