Polyclonal STAT6
- Known as:
- Polyclonal STAT6
- Catalog number:
- pc-432
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal STAT6
Related genes to: Polyclonal STAT6
- 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: Polyclonal STAT6
Related articles to: Polyclonal STAT6
- Inborn errors of immunity (IEIs) are rare diseases that affect the immune system. Variants in over 500 genes have been identified as causative of 555 IEIs, with clinical phenotypes that can be heterogeneous within the same gene or even within the same variant. Therefore, these challenges make it difficult to determine the cause of IEI in individuals with immune disorders and to link clinical phenotypes to the precise genetic damage. An incorrect diagnosis can miss approximately 25% of IEI patients with overlapping initial manifestations. Accurate diagnosis and timely treatment are essential to improving quality of life and prolonging the lives of patients, as these patients often suffer from severe, life-threatening infections if left untreated. - Source: PubMed
Publication date: 2026/05/28
Kim Lien Nguyen ThiVan Tung NguyenMinh Huong Le ThiVan Anh Nguyen ThiPhuong Mai Nguyen ThiDien Tran MinhHien Nguyen ThanhTao Nguyen ThienHoang Nguyen Huy - Alzheimer's disease (AD) is a progressive neurodegenerative disorder, which has recently been found to be closely associated with neuroinflammation. As an anti-inflammatory drug, triptolide (TP), a natural diterpenoid from , was selected in the current study for treating PS19 (tau transgenic) mice, tauopathy AD mice. In addition, we have previously found that TP had the ability to reduce the level of cholesterol. However, the roles and mechanisms of TP in the above processes are not clear. To this end, we found that elevated cholesterol in serum and brain tissues upregulated the expression of apolipoprotein E (APOE) and sialic acid-binding Ig-like lectin 3 (CD33), leading to the activation of SH2-containing protein tyrosine phosphatase 1 (SHP-1). The activation of SHP-1 inhibits the signaling pathways of Janus kinase 1 (JAK1) and signal transducer and activator of transcription 6 (STAT6), which results in inhibition of the M2 polarization of microglia, which exacerbates neuroinflammation and cognitive decline in high-cholesterol diet (HCD)-fed mice. Conversely, TP treatment significantly inhibited the hepatic sterol regulatory element-binding protein 2 (SREBP2)/3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) pathway, which reduced the cholesterol levels in the serum and brain. By depressing the levels of cholesterol, the axis of CD33 and SHP-1 was suppressed, which resulted in restoration of the activity of JAK1 and STAT6 pathways, leading to the transition of microglia from the M1 to the M2 phenotype. Of note, these observations demonstrate that TP alleviates the cognitive impairment of PS19 mice via depressing neuroinflammation. Altogether, our results revealed the mechanisms of TP in treating AD via CD33/SHP-1/JAK1/STAT6 pathways in a cholesterol-dependent manner. - Source: PubMed
Publication date: 2026/05/22
Yang YiMa YueWang PuGuan Pei-Pei - The research focused on investigating the function and underlying mechanisms of Danggui Shaoyao San (DSS) in nephrotic syndrome (NS). The NS rat model was established using doxorubicin (Dox), and 24-hour urinary protein (UP) level was measured in NS rats. Blood urea nitrogen (BUN) and serum creatinine (SCr) levels were detected using an automatic biochemical analyzer; morphological changes of renal tissues were observed by HE staining; serum interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) levels were measured by ELISA; and the protein expression of interleukin 13 (IL-13), signal transducer and activator of transcription 6 (STAT6), phospho signal transducer and activator of transcription 6 (p-STAT6) was evaluated by Western blot. NS cell model was established using Dox. Cell viability was detected by MTT, and apoptosis was detected by flow cytometry. DSS reduced UP, BUN, and SCr levels and also decreased serum IL-6, IL-1β, and TNF-α levels in NS rats in a dose-dependent manner. Renal tissue injury in NS rats was significantly lessened by DSS. Finally, DSS increased cell viability and decreased apoptosis. In a dose-dependent manner, DSS led to a dose-dependent inhibition of IL-13 and p-STAT6 protein expression. DSS alleviates NS by inhibiting IL-13/STAT6 axis activation. - Source: PubMed
Publication date: 2026/06/10
Zhang T ZQin M - Muscle regenerative capacity declines with aging and disease, which leads to muscle loss and reduced lifespan. Muscle regenerative failure is related to a disrupted network orchestrated by multiple muscle-harbored cell types; whether and how the interplay between macrophages and myofibers contributes to this process is largely unknown. Herein, we report upregulation of histone methyltransferase G9a in both aged human muscle and mouse muscle after injury. Deletion of G9a in either myeloid cells or myofibers accelerates muscle regeneration. Mechanistically, G9a down-regulates macrophage-derived interleukin 13 (IL13) and suppresses myofiber-derived myokine musclin, respectively, to inhibit myogenesis and macrophage phenotype transition during muscle regeneration. Either IL13 or musclin, per se, accelerated muscle regeneration, and their combined administration showed synergistic effects with therapeutic potentials for muscle degeneration disorders. Collectively, we highlight a crosstalk between macrophages and myofibers through IL13-Stat6 signaling and musclin, both regulated by G9a, which steers a pro-recovery microenvironment after muscle injury, with therapeutic potentials for muscle degeneration disorders. - Source: PubMed
Publication date: 2026/06/10
Jin YingZhou KaiyangHao SiyuYue HuWang HaoyuLiu ZhiyuanZhou YihaoXie YunhaoLiu XinranChen HongLiu YuxiaPeng AnlinLi YangkaiHuang KunZheng Ling - Solitary fibrous tumor (SFT) is a fibroblastic neoplasm with NAB2 and STAT6 gene fusion as well as STAT6 nuclear expression. Uncommon variants of intracranial SFTs, such as glandular and papillary structures, are extremely rare. We present a rare SFT case in a 64-year-old female demonstrating unprecedented glandular structures and extensive myxoid stromal changes. This morphologic divergence underscores the imperative for molecular validation in SFTs with atypical histologic features. Our findings advocate a refined diagnostic protocol: RNA-based next-generation sequencing (RNA-NGS) must be prioritized in STAT6-immunopositive central nervous system (CNS) mesenchymal tumors when DNA-NGS fails to identify the pathognomonic NAB2::STAT6 fusion, as demonstrated by the resolution of diagnostic ambiguity through detection of a cryptic NAB2-exon4::STAT6-UTR fusion in this case. - Source: PubMed
Publication date: 2026/05/25
Xu TingtingZheng ShashaWang Leiming