Stat1 _ Stat3 EMSA Probe Set
- Known as:
- Stat1 _ Stat3 EMSA Probe Set
- Catalog number:
- AY1404P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- Stat1 _ Stat3 EMSA Probe Set
Related genes to: Stat1 _ Stat3 EMSA Probe Set
- 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
- Gene:
- STAT3 NIH gene
- Name:
- signal transducer and activator of transcription 3
- Previous symbol:
- -
- Synonyms:
- APRF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: Stat1 _ Stat3 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: Stat1 _ Stat3 EMSA Probe Set
- This study aimed to evaluate the therapeutic efficacy of Compound Nanxing Zhitong Plaster (CNZP) against rheumatoid arthritis (RA) and to investigate its underlying mechanism through an integrated approach combining network pharmacology and metabolomics. - Source: PubMed
Publication date: 2026/09/03
Li ZhiqiangCao LiangWang JiajiaGao XiaSuo FengtaiLuo FengshouXu WentaoWang ZhenzhongZhang XinzhuangXiao Wei - Systemic lupus erythematosus (SLE) and other chronic inflammatory diseases are complex, multifactorial conditions where patient heterogeneity poses a major challenge to treatment. Despite the availability of numerous omics technologies, reliable biomarkers for precision medicine remain scarce, and many cell-based approaches are difficult to integrate into clinical settings. In this proof-of-concept study, we hypothesized that interrogating the cells' imprinting by the inflammatory environment through Unperturbed Activation Profiling (UACT) without prior restimulation would allow for the assessment of individual immune status in chronic rheumatic diseases. - Source: PubMed
Publication date: 2026/08/17
Burns MarieOstendorf LennardAbbas AmroFerrara SebastianHirseland HeikeBaumgart SabineBarreno-Sanchez AdrianFrischbutter StefanAlexander TobiasBiesen RobertMei Henrik EGrützkau AndreasSchulz Axel R - Visceral leishmaniasis (VL) is associated with impaired Th1 responses, yet the intracellular signalling events linking immunosuppressive pathways to effector dysfunction remain poorly defined. We studied 150 adults in endemic northern Nigeria (50 active VL, 50 healed VL, 50 endemic controls) using flow cytometry, cytokine profiling, targeted RT-qPCR of 13 JAK-STAT pathway genes with dual reference gene normalisation, ex vivo checkpoint blockade, and phospho-flow cytometry for STAT1/STAT3 in both CD4+ T cells and CD14+ macrophages. Active VL was associated with reduced antigen-specific IFN-γ (220 versus 940 pg/mL in healed VL; P < 0.001), elevated IL-10, expanded regulatory T cells, transcriptional upregulation of STAT3 (2.66-fold, adjusted P < 0.001), and downregulation of its negative regulator SOCS3 (0.56-fold, adjusted P = 0.001). A STAT3-dominant phosphorylation profile was present in both CD4+ T cells (pSTAT1/pSTAT3 ratio 1.33) and, more prominently, CD14+ macrophages (ratio 0.51; Kruskal-Wallis P < 0.001 across disease groups). CD14+ pSTAT3 correlated with macrophage infection index (Spearman ρ = 0.52, P < 0.001), linking signalling state to effector function. Combined IL-10 and PD-1 blockade reversed the signalling imbalance in both compartments, restored IFN-γ production up to 4.8-fold, and reduced macrophage infection index by 42%. Pharmacological STAT3 inhibition with Stattic confirmed pSTAT3 reduction by phospho-flow cytometry (-33%, P < 0.001), reproduced transcriptional reprogramming comparable to checkpoint blockade for 9 of 13 genes, and enhanced macrophage parasite clearance (infection index -36%, P < 0.001). These findings across phosphoprotein, transcript, and functional levels identify a STAT3-dominant signalling signature spanning T-cell and macrophage compartments as a consistent feature of immune suppression in human VL and a candidate therapeutic target warranting investigation. - Source: PubMed
Publication date: 2026/08/24
Asaga Peter MacKroeger AxelAirohuodion PhilomenaAnyaike ChukwumaBako IshakuMakpo JamesBuba DeborahDanaan Dakul Anthony - Antigen-specific humoral responses are critical for long-term protection against infectious diseases, yet the mechanisms that regulate B cell differentiation and antibody production remain incompletely defined. Here, we identify the Protein Tyrosine Phosphatase Nonreceptor Type 2 (Ptpn2) as a B cell-intrinsic regulator of plasma cell fate and isotype switching. Using a B cell-specific Ptpn2 knockout mouse model, we show that Ptpn2 restrains both B cell receptor and interferon-γ (IFN-γ) signaling by directly dephosphorylating Lyn, STAT1, and STAT3. Loss of Ptpn2 leads to hyperactivation of these two signaling pathways, resulting in transcriptional reprogramming that promotes plasma cell differentiation and increased IFN-γ-driven antibody production. Functionally, Ptpn2-deficient mice generated enhanced primary antiviral antibody responses following influenza infection and elevated virus-specific and neutralizing titers upon recall without compromising affinity. These findings identify Ptpn2 as a key intracellular checkpoint that integrates antigenic and inflammatory cues to regulate humoral immunity, with potential implications for enhancing vaccine-induced protective immunity. - Source: PubMed
Publication date: 2026/08/19
Hincapie Ana MariaPoirier AlexandreAubry IsabelleAumont PhilippeBhagrath AanyaUetani NorikoColalillo BiancaWu ChenyueCharbonneau BenoitBussieres-Marmen StephanieAbidin Belma MDi Noia Javier MMandl Judith NVidal Silvia MFritz Jorg HTremblay Michel L - C-C motif chemokine ligand 2 (CCL2) contributes to post-traumatic neuroinflammation and blood-brain barrier (BBB) disruption, but its role in post-traumatic external cerebral herniation and endothelial JAK-STAT signaling remains unclear. - Source: PubMed
Publication date: 2026/08/14
Chen QizuanXia JinbiaoZhang ShangmingPei JiashengLi ZiqiLiu ZhengWei LiangfengWang Shousen