Stat1 p84_p91 Luciferase Reporter Vector
- Known as:
- Stat1 p84_p91 Luciferase Reporter Vector
- Catalog number:
- LR0075
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- Stat1 p84_p91 Luciferase Reporter Vector
Related genes to: Stat1 p84_p91 Luciferase Reporter Vector
- Gene:
- STAT1 NIH gene
- Name:
- signal transducer and activator of transcription 1
- Previous symbol:
- -
- Synonyms:
- STAT91, ISGF-3
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: Stat1 p84_p91 Luciferase Reporter Vector
Related articles to: Stat1 p84_p91 Luciferase Reporter Vector
- Defined polysaccharide fractions can reshape the gut microbiome and influence systemic antitumor immunity. We investigated whether an operationally defined high-molecular-weight Polygonatum sibiricum polysaccharide fraction (PSP-H) enriched by 100 kDa ultrafiltration suppresses growth of subcutaneous MC38 tumors via microbiota-dependent mechanisms and potentiates anti-PD-1 therapy. - Source: PubMed
Publication date: 2026/06/19
Wang YonghengWu XinhongDeng HaibinYan GuiyingXu ZhenyeZhu Limin - Cold exposure is an important environmental risk factor for adverse cardiovascular outcomes, but the immune mechanisms linking cold stress to myocardial injury remain incompletely defined. Here, we investigated whether curcumin protects the cold-stressed heart by regulating macrophage polarization and the STUB1/STAT1-STAT6-KLF4 signaling network. Using a severe intermittent mouse cold-exposure model and a mild hypothermic BMDM cold-mimic system, we found that cold stress impaired cardiac function, increased inflammatory infiltration, and shifted macrophages toward a pro-inflammatory phenotype. Cold mimicry enhanced STUB1-STAT1 interaction and K48-linked STAT1 ubiquitination, reduced STAT1 abundance, and was accompanied by suppression of STAT6 activation and KLF4 transcription. Given the canonical antagonism between STAT1- and STAT6-driven macrophage programs, these changes are interpreted as context-specific co-disruption of STAT-family signaling under cold-induced proteostatic/inflammatory stress, rather than as evidence that STAT1 degradation alone directly suppresses STAT6. Curcumin reduced STUB1 abundance and STUB1-STAT1 engagement, attenuated STAT1 ubiquitination, restored STAT6 nuclear signaling and STAT6-dependent Klf4 transcription, and promoted anti-inflammatory macrophage polarization. In a species-matched Transwell co-culture system, curcumin-treated macrophages reduced inflammatory cytokine release and improved cardiomyocyte viability through paracrine effects. Macrophage-specific Klf4 deletion markedly attenuated curcumin-mediated immune remodeling and cardioprotection in vivo. These findings identify a macrophage-centered signaling network that contributes to cold stress-induced myocardial injury and position curcumin as an experimental immunomodulatory candidate. However, direct curcumin-STUB1 target engagement, systemic cytokine changes, optimal dosing/formulation, and human efficacy remain to be established. - Source: PubMed
Publication date: 2026/06/19
Cong PeifangTong ChangciLiu JinpengLuo ZhonghuaLi HaikunYao JianLiu Yunen - Gain-of-function (GOF) mutations in the STAT1 gene result in heightened interferon signaling and impaired IL-17 immunity. While chronic mucocutaneous candidiasis (CMC) remains the hallmark feature, affected individuals often display a broader phenotype including viral infections, mycobacterial susceptibility, and autoimmune diseases. - Source: PubMed
Publication date: 2026/06/19
Arslan SerkanSert AhmetÖzçelik MeryemBarış SafaAydoğmuş ÇiğdemKaba ÖzgeÇil Yılmaz BurcuErdil SimgeYırgın KübraGökmirza PınarÇatak Mehmet Cihangir - Wilson disease (WD) is characterized by hepatic injury caused by copper accumulation; however, the underlying molecular mechanisms remain incompletely understood. This study aims to investigate whether copper overload induces pyroptosis in WD and to elucidate the role of USP9X-mediated JAK1 deubiquitination in this process. - Source: PubMed
Publication date: 2026/06/18
Zi HuaduanTang HengchengYang XiaoxiLi XiaojinLi YanmengXu AnjianOuyang QinChen SisiHe PingpingLi YanlingZhu QianyuZhang BeiZhang WeiOu XiaojuanSun LiyingZhou DonghuHuang Jian - Type 1 diabetes (T1D) has traditionally been viewed as an immune-driven disease. However, evidence from pre-onset T1D individuals suggests that pancreatic β-cells show reduced metabolic gene expression and stress responses before substantial immune entry. In this review, we examine how chronically stressed β-cells are detectable in a reshaped local microenvironment prior to overt immune cell infiltration, a period defined as a "pre-immune" niche. During this period, pre-onset β-cells exhibit early extracellular matrix (ECM) remodeling capabilities, endoplasmic reticulum and Golgi stress, a shift in their soluble-factor secretome and extracellular outputs, including release of extracellular vesicles with distinct cargo. Loss of the double C2-like domain containing protein B (DOC2B), a regulator of vesicle trafficking and membrane fusion, may contribute to these processes. Beyond its canonical role in regulated insulin exocytosis, DOC2B negatively regulates cytokine-induced CXCL10 expression in β-cells via inhibition of IKKβ-STAT1 signaling, and its loss increases activation of these pathways. DOC2B loss in cancer models promotes the formation of filopodia, protrusive structures capable of ECM engagement for matrix metalloproteinase-mediated degradation; similarly, we consider whether changes in β-cells could influence maladaptive interactions with the peri-islet matrix during early T1D. Together, these concepts position DOC2B as a potential additional point of β-cell vulnerability; further study may help guide early biomarker development and inform long-term strategies for intercepting T1D before clinical onset. - Source: PubMed
Esparza DianaJayasena Chathurani SJovanovic-Talisman TijanaThurmond Debbie C