STAT4 TAD in vivo Kinase Assay Kit
- Known as:
- STAT4 TAD vivo Kinase Assay Kit
- Catalog number:
- LK0020
- Product Quantity:
- 10ug
- Category:
- Peptides
- Supplier:
- Panomics
- Gene target:
- STAT4 TAD vivo Kinase Assay Kit
Related genes to: STAT4 TAD in vivo Kinase Assay Kit
- Gene:
- STAT4 NIH gene
- Name:
- signal transducer and activator of transcription 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q32.2-q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2018-02-13
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- Due to the complexity of clinical work, some blood samples for lymphocyte activity detection might be conducted thrice weekly rather than daily. Whether the levels of cytokines secreted by lymphocytes are affected by storage time of blood samples has not been studied. In clinical work, we found that many samples that were not tested on the day of blood collection had lower levels of interferon secretion than normal. Consequently, we assessed cell counts and cytokines secreted by lymphocytes across varying storage time by flow cytometry to study the changes in cytokine expression and to determine optimal sample processing timing. We found that with the extension of storage time, the proportion and absolute count of various lymphocytes were significantly decreasing. Particularly, natural killer cells (NK cells), CD4 T cells, CD8 T cells and NKT-like cells all showed a decreased interferon γ (IFN-γ) secretion as early as the second day of blood collection. The levels of TNF-α secreted by CD8 T cells and NKT-like cells also decreased with storage time. The expression of granzyme B and perforin by various lymphocytes did not change within the 7-day storage period. Moreover, prolonged storage time markedly reduced the phosphorylation of signal transducer and activator of transcription 4 (STAT4) in lymphocytes, which was accompanied with decreased IFN-γ secretion. Our results indicated that failure to perform timely testing would lead to inappropriate understanding of cell quantity and state in clinical practice. This study provides a reference for clinical choice of optimal sample testing time, thereby minimizing potential biases introduced by suboptimal storage time. - Source: PubMed
Publication date: 2026/08/07
Huang RuoyuLiu XuDai XiaoranYu XiaojingXu YuanhongZheng YuanlingZong Lu - : Novel Sézary syndrome (SS) biomarker genes identified previously through transcription profiling were examined for changes in expression after mogamulizumab treatment. Incorporating new biomarkers for measuring response to disease would improve clinical care. : To assess novel SS biomarker and cytokine genes in patients treated with mogamulizumab with clinical response, blood response, and immunologic parameters. : We performed a real-world case-control and case-case study analyzing the expression of SS biomarker genes in peripheral blood mononuclear cells (PBMCs) from six SS patients treated with mogamulizumab using qRT-PCR. : We demonstrated a reduced expression of SS biomarker genes in PBMCs of SS patients following mogamulizumab therapy. In our cohort, five of the SS biomarker genes (, , , and ) showed statistically consistent high expression compared to normal PBMCs at baseline. After treatment with mogamalizumab, these five SS biomarkers showed significant correlations with skin response ( < 0.05) and three (, and ) with blood response ( < 0.05). A decrease in expression correlated to an improvement in skin severity, and inversely correlated to Sézary cell decrease ( < 0.05). Two cytokine genes, and , reflective of an immune response that is abnormal in SS, showed a trend to normalized expression with decreasing and increasing after treatment. : This was a real-world study of patients who failed prior treatments, with a small sample size and variable timing between patient sample collection. : Unique SS biomarker, cytokine and T cell transcription factor genes are valuable in assessing molecular and immune responses following treatment. - Source: PubMed
Publication date: 2026/07/17
Davis AlannaYing JunHsu Ping-ChingChen JeffreyTran KhiemWong Henry K - Hepatocellular carcinoma (HCC) arises through heterogeneous pathways involving chronic hepatitis B virus infection, hepatitis C virus infection, alcohol-related liver disease, metabolic dysfunction-associated steatotic liver disease, fibrosis, cirrhosis, and environmental exposures. Genome-wide association studies (GWASs) have identified host germline loci associated with HCC susceptibility, but interpretation is complicated by aetiology, ancestry, liver disease stage, and the definition of controls. This narrative review examines current GWAS evidence for HCC, with emphasis on aetiology-specific susceptibility, functional interpretation, cross-disorder genetic effects, and clinical translation. - Source: PubMed
Publication date: 2026/06/30
Zhang SiweiLong Xiaohang - Spinal cord injury (SCI) leads to a complex cascade of cellular events, among which necroptosis plays a critical role in exacerbating neuronal injury and inflammation. In this study, we aimed to identify and validate key genes associated with necroptosis in SCI using bulk RNA-seq data, followed by differential analysis and weighted gene coexpression network analysis (WGCNA). We identified several candidate necroptosis-related genes, and further least absolute shrinkage and selection operator (LASSO) regression highlighted five SCI-necroptosis differentially expressed genes (DEGs): toll-like receptor 4 (Tlr4), Nlrp3, Il1b, Tnfaip3, and Stat4. These genes were validated using RT-qPCR and western blot experiments. Our analysis revealed that necroptosis scores were significantly elevated following SCI. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) analysis revealed that Tlr4 was upregulated in myeloid cells (microglia and macrophages) and played a pivotal role in triggering downstream necroptosis, which was confirmed by protein levels. In vitro and in vivo experiments confirmed that Tlr4 inhibition attenuated necroptosis and inflammation. This study is the first to establish Tlr4 as a direct upstream regulator of the pRIPK1/pRIPK3/pMLKL necroptotic axis in SCI, distinct from its role as a general inflammatory mediator, suggesting Tlr4 as a promising therapeutic target for functional recovery. - Source: PubMed
Wang WanzhouSun LuXie WeiChen FangqingHong Cheng - The tumor microenvironment (TME) plays a significant role in the development of non-small cell lung cancer (NSCLC). Tumor-associated macrophages (TAMs) are the most abundant immune cells in the TME, with M2 macrophages playing a critical role in tumor progression. Our previous studies have shown that pine needle oil and its main active component, bornyl acetate (BA), can effectively inhibit the growth of NSCLC cells. This effect is achieved by inhibiting the PI3K/AKT/ABCB1 signaling pathway. However, it remains unclear whether BA can suppress the invasion and migration of NSCLC cells by regulating the polarization of macrophages. Therefore, our research aims to further investigate the impact of BA on macrophage polarization to evaluate its potential mechanisms in inhibiting NSCLC invasion and migration. In this study, we observed a significant presence of M2 macrophages in NSCLC tumor tissues. Cell experiments indicated that BA is non-cytotoxic to M0 macrophages and can induce their polarization into M1 macrophages, thereby inhibiting the invasion and migration of NSCLC cells. Mechanistic studies revealed that BA promotes M1 polarization by upregulating the phosphorylation of p65/STAT4. Animal experiments further confirmed that BA can regulate M1 macrophage polarization and inhibit NSCLC growth. However, when we blocked the p65/STAT4 pathway, the antitumor effects of BA were lost, and tumor growth resumed. These findings suggest that BA induces M1 macrophage polarization by activating the p65/STAT4 pathway, which in turn suppresses the invasion and migration of NSCLC cells. In conclusion, this study provides a foundation for further exploration of the mechanisms of BA and other natural products and offers new insights for developing NSCLC treatments based on immune environment regulation. - Source: PubMed
Publication date: 2026/07/22
Tu ZiyiTao RongshanWang XuanyinRen JiamingYang ZeyangWang LuLu MaoqinZhang YingCao YaxuanZhu XuLi LongLiu XinleiCao YuWu Jieheng