STAT6 (Phospho_Thr645) Antibody
- Known as:
- STAT6 (Phospho_Thr645) Antibody
- Catalog number:
- E011051-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- STAT6 (Phospho_Thr645) Antibody
Related genes to: STAT6 (Phospho_Thr645) Antibody
- Gene:
- STAT6 NIH gene
- Name:
- signal transducer and activator of transcription 6
- Previous symbol:
- -
- Synonyms:
- D12S1644, IL-4-STAT
- Chromosome:
- 12q13
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-09
- Date modifiied:
- 2019-04-23
Related products to: STAT6 (Phospho_Thr645) Antibody
Related articles to: STAT6 (Phospho_Thr645) Antibody
- Previous studies indicated that cell-free RNA (cfRNA) in spent embryo medium (SEM) may serve as a noninvasive biomarker for evaluating embryonic development. However, its stage-specific expression patterns and functional dynamics during preimplantation embryos are still unclear. In view of this, this study performed transcriptome sequencing on cfRNAs from follicular fluid (FF) and SEM at different developmental stages. This result showed that the number of identified cfRNAs showed a trend of decreasing from follicular to cleavage stage, then increasing through blastocyst stage. The proportion of low abundance genes of protein coding RNA (mRNA) and long noncoding RNA (lncRNA) in FF and spent cleavage medium (SCM) was relatively high (0 < FPKM ≤ 10). The proportion of low abundance genes of mRNA and lncRNA in spent blastocyst medium (SBM) was lower than that of high abundance genes (FPKM > 10). The cfRNAs of differentially expressed were detected in FF, including ribosomal proteins and genes involved in protein translation. The genes regulating protein kinase activity were significantly enriched in SCM. Cellular signal transduction, energy metabolism, immunity, RNA transcription, and splicing genes were significantly enriched in SBM. Further studies revealed that immune genes (JAK3, STAT6, DOCK8, CD74) in SBM were closely related to embryo quality, and the expression level of immune genes in high-grade SBM (hSBM) was significantly (p < 0.05) higher than that of low-grade SBM. The Wnt/β-catenin signaling pathway was found to be associated with hSBM, potentially contributing to blastocyst development through the release of immune factors and activation of immune-related pathways. However, these findings were preliminary. Therefore, this study results provide new insights into the molecular dynamics of preimplantation embryos and the impact of immune responses on embryo quality. - Source: PubMed
Shi HuajuanSheng YuqiZhang ChunnuanPan MinLi LehanJing AihuaCai LingboGe Qinyu - The process of cellular demise is fundamental for sustaining physiological balance and influencing disease outcomes. Recently, exosomes have emerged as critical nanoscale messengers in intercellular signaling, with versatile functions in orchestrating distinct patterns of programmed cell death. This article provides a comprehensive overview of exosome-mediated regulation of multiple cell death subtypes-including apoptosis, ferroptosis, necroptosis, entosis, SLFN11-related death, and ammonia-triggered death-and highlights their multifaceted contributions to immune modulation, cancer development, and tissue regeneration. This article integrates Ongoing studies on the functions of exosomes in various cell death modes from the perspectives of signaling pathways, epigenetic regulation, and metabolic pathways. It focuses on the molecular mechanisms by which exosomes, through bioactive cargos such as miRNA, lncRNA, circRNA, and proteins, influence key signaling axes, including PI3K/AKT, Fas/FasL, p53, SLC7A11/GPX4, RIPK1/RIPK3/MLKL, Keap1/Nrf2, STAT6, and TAM receptors. Notably, exosomes demonstrate powerful specificity and systemic regulatory potential, particularly in the regulation of iron homeostasis, lipid peroxidation, immune polarization, and entosis. As a "nano delivery system" for intracellular and extracellular signals, exosomes not only regulate cell death modalities but also offer new strategic possibilities for disease intervention. In the future, exosome-mediated cell death regulation is expected to be used in the development of precision therapeutic tools, improving the intervention efficiency in tumors, immune diseases, and metabolic disorders. In summary, a thorough insight of the mechanisms by which exosomes regulate cell death is crucial for elucidating the fundamental basis of disease development and for translational medical applications. - Source: PubMed
Publication date: 2026/05/12
Zhang LanyueSu LanqianZhao JiangnanXu JiayuXu KeChi Hao - Solitary fibrous tumour is an uncommon, predominantly benign tumour of mesenchymal origin, developing mainly in the thoracic cavity and on the pleural surface, although it has been reported in a wide variety of extrapleural sites. Its occurrence in the liver is particularly rare. We present the case of a 57-year-old woman in whom a large mass was identified in the left lobe of the liver, demonstrating inhomogeneous contrast enhancement without significant compression of the abdominal vessels. The lesion measured 170 mm in its greatest diameter and severely destroyed the surrounding liver parenchyma. SFT is characterised by haphazardly arranged ovoid and spindle-shaped cells with numerous mildly staghorn-like vessels lined by flattened endothelium. It typically shows gene rearrangement with CD34 and/or STAT6 positivity on immunohistochemistry. Since imaging methods are not specific regarding the nature of the lesion, pathological and immunohistochemical analyses are essential for establishing an accurate diagnosis and assessing differential diagnostic possibilities. - Source: PubMed
Publication date: 2026/04/23
Gráczer AlexandraLantos TamásSejben Anita - Immunotherapies have been widely applied to the treatment of hepatocellular carcinoma (HCC), but to date only a minority of patients exhibit dramatic responses. Tumor-associated macrophages (TAMs) are vital components in the tumor microenvironment and are involved in HCC progression. Herein, we confirm the upregulation of PCBP1 expression in TAMs correlates with poor prognosis in HCC patients. The loss of PCBP1 in TAMs promotes M1 like macrophages polarization and suppresses the migration capability of HCC cells in vitro. Additionally, overexpression of PCBP1 increases M2 macrophage infiltration and promotes tumor growth in vivo. Mechanistically, PCBP1 negatively regulates autophagy flux induction in TAMs to hinder STAT6 degradation from autophagy pathway, thereby facilitating M2-like macrophage phenotype and HCC malignant progression. Collectively, our findings describe the role of PCBP1 in orchestrating TAMs polarization and suggest that blocking PCBP1 is an effective approach in combating the cancerous advancement of HCC. - Source: PubMed
Publication date: 2026/05/10
Luo YueZhang XinyuYang HaoyiYao YuxinWu HaoZhang ZhuYe DongjiePan BanglunWang XiaoqianTang Nanhong - Alzheimer's disease (AD) is characterized by progressive memory decline and neuronal loss, driven primarily by dysregulated inflammatory signaling. Signal transducer and activator of transcription 6 (STAT6) is a member of the STAT family and has been implicated in the progression of various diseases. This study aimed to investigate whether inhibiting STAT6 and its downstream target, suppressor of cytokine signaling 2 (SOCS2), could mitigate Aβ1-42-induced neuronal injury in both cellular and animal models of AD. AD-like pathology was induced in Sprague-Dawley rats (n = 10 per group) by intracerebral administration of amyloid β1-42 (Aβ1-42). Radial arm maze test, elevated plus maze test, and passive avoidance task were performed to estimate cognitive impairments of AD rats. H&E and TUNEL staining were performed to analyze pathological changes as well as neuron loss and apoptosis. HT-22 neuron cells were exposed to Aβ1-42 to establish an AD-relevant in vitro model. Cell viability and apoptosis were evaluated via CCK-8 and flow cytometry. Bax and Bcl-2 levels were estimated by Western blotting. Reactive oxygen species (ROS) production was measured using the DCFH-DA assay. ChIP and luciferase reporter assays were performed to assess the interaction between STAT6 and SOCS2 promoter. The results showed that STAT6 expression was significantly upregulated in the hippocampus of rats following Aβ1-42 infusion. Silencing of STAT6 alleviated Aβ1-42-induced cognitive impairments in AD rats by significantly reducing neuronal apoptosis (as evidenced by fewer TUNEL-positive cells), attenuating oxidative stress (indicated by reduced MDA levels and restored activities of antioxidant enzymes SOD and GSH-Px), and downregulating SOCS2 levels in vivo. Consistently, in vitro experiments demonstrated that STAT6 knockdown in HT-22 hippocampal neurons markedly inhibited Aβ1-42-triggered apoptosis, intracellular ROS accumulation, and oxidative stress marker dysregulation, whereas overexpressed STAT6 exerted an opposite role. Notably, STAT6 was found to bind to the SOCS2 promoter region. Functionally, SOCS2 overexpression alone accelerated HT-22 cell injury, and critically, it abolished the neuroprotective effects conferred by STAT6 depletion, specifically reversing the suppression of apoptosis and oxidative stress. These findings implicate that the STAT6-SOCS2 axis contributes to AD pathology, and their inhibition exerts neuroprotective effects. - Source: PubMed
Publication date: 2026/05/12
Liu YuPeng LangLi MingYan WenjingXiang Qingwei