Polyclonal STAT2
- Known as:
- Polyclonal STAT2
- Catalog number:
- pc-430
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal STAT2
Related genes to: Polyclonal STAT2
- Gene:
- STAT2 NIH gene
- Name:
- signal transducer and activator of transcription 2
- Previous symbol:
- -
- Synonyms:
- STAT113
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: Polyclonal STAT2
Related articles to: Polyclonal STAT2
- Osteoblast development must be precisely regulated, as insufficient bone formation results in low bone mass and skeletal fragility, whereas excessive osteogenesis drives heterotopic ossification (HO), the ectopic formation of bone in soft tissues. Here, we identify the deubiquitinating enzyme ubiquitin-specific peptidase 24 (USP24) as a key regulator of both physiological and pathological ossification. USP24 is highly expressed in skeletal tissues, where it promotes osteoblast development by stabilizing STAT2 through deubiquitination. Loss of USP24 reduces osteoblast differentiation and bone formation, an effect mirrored by STAT2 deficiency. Beyond physiologic bone, USP24 and STAT2 are also strongly expressed in heterotopic bones from patients with HO. In a fibrodysplasia ossificans progressiva (FOP) mouse model, recombinant adeno-associated virus (rAAV)-mediated silencing of Usp24 markedly diminished HO pathogenesis and reduced STAT2 protein levels in HO lesions. Consistently, USP24 deficiency attenuated activin A-induced bone morphogenetic protein (BMP) signaling and osteogenesis, with comparable effects observed upon Stat2 silencing. Together, these findings uncover a previously unrecognized role for USP24-STAT2 signaling in osteoblast differentiation and HO, highlighting bone-targeted USP24-STAT2 inhibition as a potential therapeutic strategy for pathologic bone formation. - Source: PubMed
Publication date: 2026/05/30
Kim Jung-MinYang Yeon-SukXie JunKang Chan MiCho Yeong-ChanPark Kwang HwanGong FengSato TadatoshiKim Beom-JikGao GuangpingShim Jae-Hyuck - Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organ systems. In SLE, T-cell subsets are closely associated with autoimmunity and organ inflammation. Detecting T-cell exhaustion (TEX)-related biomarkers is crucial for early SLE diagnosis and offers new insights into disease mechanisms. Transcriptomic data for SLE were collected from public databases, and TEX-related genes were obtained from the literature. Biomarkers were identified using analyses such as differential expression analysis and machine learning algorithms. The potential mechanisms of action of these biomarkers were further investigated, including nomogram construction, gene set enrichment analysis, immune microenvironment analysis, molecular regulatory network analysis, molecular docking, and reverse transcription-quantitative polymerase chain reaction validation. IFIT3, IFIH1, CXCL10, and STAT2 were identified as biomarkers. The nomogram demonstrated good predictive performance. These biomarkers were mainly involved in biological processes such as ribosome biogenesis and negative regulation of viral genome replication. Four significantly different immune cell types were identified, including monocytes and resting memory CD4 T cells. The biomarkers were found to be regulated by several transcription factors and microRNAs. Furthermore, the 4 biomarkers exhibited high binding affinity for several drugs; in particular, the binding energy of STAT2 with bisphenol A was -7.0 kcal/mol. Finally, reverse transcription-quantitative polymerase chain reaction results showed that all 4 biomarkers were significantly upregulated in SLE patients. In summary, this study identified TEX-related biomarkers in SLE, which may have important clinical implications for the diagnosis and treatment of SLE. - Source: PubMed
Yang LanqingGao WeiYang LuluLiu Xingyu - Sepsis has a high mortality rate, yet the cellular heterogeneity and transcriptional regulatory programs associated with divergent clinical outcomes remain incompletely understood. Here, we integrated two peripheral blood single-cell RNA-seq cohorts to explore prognosis-associated immune remodeling patterns in sepsis. Using reference-based annotation, pySCENIC-inferred regulon activity, pathway enrichment, and CellChat based ligand-receptor inference, we observed broad differences in cell composition, transcriptional programs, and intercellular communication between survivors and non-survivors. Non-survivors exhibited relative decrease of monocytes, B-cells, NK cells, and CD4/CD8 T cells, together with relative platelet expansion. cDC2 and plasmablasts showed relatively large transcriptional disturbance compared to other cell types. In cDC2, poor outcome was associated with increased TNF-α and NF-κB related regulon activity, which linked to AP-1 transcription factors (JUN, FOSL2, CEBPB, NFIL3, KLF6, and FOSB), together with reduced STAT1 and STAT2-associated interferon signaling. Gene regulatory network analysis highlighted cell type-specific transcription factor and target gene relationships. CellChat suggested that cDC2 may occupy a more connected position in survivors, whereas connectivity appeared reduced in non-survivors. Independent bulk transcriptomic validation supported increased FOSL2 and CEBPB expression, and a multivariable eight-transcription-factor model showed preliminary discriminatory performance. Overall, this study suggests that poor-outcome sepsis may be associated with altered cDC2 regulatory states and reduced cDC2 centered intercellular coordination. - Source: PubMed
Publication date: 2026/05/29
Yang YuanmingHua YiweiYang SuyiLiu NanLi Jun - Lambda interferons signal through the interferon lambda receptor-1 (IFNLR1) and IL10RB heterodimer to induce interferon stimulated genes (ISGs). We previously showed that proteins derived from distinct IFNLR1 splice isoforms uniquely influence gene expression and HBV replication in stem cell-derived hepatocytes (iHeps). Here, we evaluated signal transduction mechanisms of full-length IFNLR1 (variant 1) and a truncated variant missing part of the cytoplasmic JAK1-interacting domain (variant 2). - Source: PubMed
Publication date: 2026/05/29
Novotny Laura AMartinez-Morant CarlaDuncan Stephen ATraktman PaulaGooz MonikaMeissner Eric G - While adaptive humoral immunity and type I interferon (IFN-I) responses are known to cross-regulate each other during viral infection, the mechanisms by which antibodies (Abs) or immune complexes (ICs) modulate IFN-I signaling in immune cells remain unclear. Here, using plate-coated human IgG (cIgG) as an antigen-independent IC mimic, we show that FcγRIIa cross-linking in human blood monocytes induces the expression of TRIM54, an E3 ubiquitin ligase previously thought to be constitutively expressed only in muscle tissue. Mechanistically, TRIM54 binds to and promotes the ubiquitination of the transcriptional activator STAT2, thereby dampening the expression of many IFN-stimulated genes. This inhibitory role is functionally corroborated by a positive correlation between elevated TRIM54 levels and enhanced cellular permissiveness to infection by vesicular stomatitis virus, Dengue virus, and/or Sendai virus, in cIgG-primed human monocytes, and monocytic cell lines with genetically modulated TRIM54 expression. Clinically, elevated TRIM54 expression is detected in circulating monocytes from pediatric patients with Epstein-Barr virus-induced infectious mononucleosis. Together, our findings define a previously unrecognized FcγRIIa-TRIM54-STAT2 signaling axis through which virus-specific Abs-particularly at sub-neutralizing concentrations-can attenuate the IFN-I response in innate immune cells. This axis may also provide a mechanistic explanation for Ab-dependent enhancement of viral infection. - Source: PubMed
Publication date: 2026/05/29
Dai Xiao-QiuHua ShenghaoXue LianGong ZhengPan Ya-YingLi ZhenjunHan ChaojieGao Xiao-MingGong Fang-Yuan