Ask about this productRelated genes to: SERPINB2 Blocking Peptide
- Gene:
- SERPINB2 NIH gene
- Name:
- serpin family B member 2
- Previous symbol:
- PLANH2, PAI2
- Synonyms:
- HsT1201
- Chromosome:
- 18q21.33-q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-02-07
- Date modifiied:
- 2018-02-13
Related products to: SERPINB2 Blocking Peptide
Related articles to: SERPINB2 Blocking Peptide
- Muscle fibrosis is a key pathological feature of Duchenne muscular dystrophy (DMD) and is closely associated with disease progression. Fibroadipogenic progenitors (FAPs) are major contributors to fibrosis, yet the precise mechanisms remain unclear. To investigate FAP dynamics and lineage specification, we generated dual-reporter mice (PRURD2) by crossing D2.B10-Dmdmdx/J (D2-mdx) mice with FAP and brown/beige adipose tissue (BAT) reporter lines. Corresponding control mice (PRURDBA) were established on the DBA/2J background. At 12 months, heart, diaphragm, and tibialis anterior (TA) muscles were collected for histological analysis. FAPs were isolated via FACS and subjected to single-cell RNA sequencing. PRURD2 mice exhibited increased fibrosis across all muscles compared to controls ( < 0.01) and a significant rise in PDGFRα-GFP + FAPs ( < 0.05). UMAP clustering identified 11 distinct FAP subpopulations, with the fibrosis-associated CD55 cluster enriched in PRURD2 mice. Pseudotime analysis showed lineage progression from progenitor clusters toward the fibrogenic CD55 cluster. CellChat analysis indicated increased interactions in PRURD2 mice involving fibrosis-related pathways like COLLAGEN, TGF-β, WNT, NOTCH, and ANGPTL. Additionally, fibrosis-related signaling pathways such as THY1, TWEAK, EPHA, EPHB, and SEMA6 showed increased interactions among FAP clusters in PRURD2 mice. Differential gene expression analysis revealed top upregulated genes including , , and . PRURD2 mice develop severe fibrosis in skeletal and cardiac muscle, driven by FAP-induced signaling pathways and genes. This model is valuable for understanding muscle fibrosis in DMD and developing anti-fibrotic therapies. - Source: PubMed
Publication date: 2026/04/24
Fusagawa HiroyoriLau JustinSharma SankalpLiu MengyaoSamimi YusefFranchet-Schaer GabrielFang AshleyFusagawa MinamiKim HubertFeeley Brian TLiu Xuhui - - Source: PubMed
Publication date: 2026/04/17
Vasamsetti Sathish BabuSadaf SamreenUddin Mohammad AShen JixingJohny EbinMondal AwishiFlorentin JonathanLei LiqunMannan AleefRao Krithika SudhakarSembrat JohnRojas MauricioSipula IanKastroll JakeJurczak Michael JShiva SrutiO'Doherty Robert MYechoor VijayDutta Partha - : Head and neck tumors have been associated with varying risks for venous thromboembolism (VTE). Through a cross-tumor comparison, we assessed site-specific coagulation-related gene expression changes in head and neck squamous cell carcinoma (HNSCC) compared to squamous cell tumors in the esophagus (ESCCa) and lung (LUSC). Further, we assessed the relationship between clinicopathologic features of HNSCC and coagulome gene expression. : RNA-sequencing data from primary tumor tissues of HNSCCa, ESCCa, and LUSC were obtained from The Cancer Genome Atlas (TCGA). Three previously identified pro-thrombotic genes (, , and ) were analyzed and, for pan-cancer comparisons, gene expression was Z-standardized and summarized as a composite coagulome score. For HNSCCa-specific analyses, gene expression was compared using log2 RSEM counts, contrasting between HPV status, primary tumor site, tumor stage, grade, and demographic characteristics. : HNSCCa demonstrated the highest composite coagulome activation (mean Z-score = 0.29, 95% CI: 0.23-0.35) compared with LUSC and ESCCa (mean Z-scores = -0.27 and -0.16, respectively; < 0.001). Among 487 HNSCCa tumors, HPV-negative tumors exhibited significantly higher composite coagulome expression than HPV-positive tumors (mean ± SD, 11.25 ± 1.39 vs. 10.14 ± 1.30; < 0.001). Oral cavity tumors demonstrated the highest coagulome expression, while oropharyngeal tumors were most suppressed. Higher histologic grade was inversely associated with coagulome expression ( < 0.001). Patient age, sex, and race were not significantly associated with coagulome expression. : HNSCCa exhibits a tumor-specific pro-thrombotic expression profile with substantial heterogeneity driven by HPV status and primary tumor site. Despite elevated tumor-specific pro-coagulant signaling, these findings reflect tumor-specific pro-thrombotic potential rather than clinical VTE risk in HNSCCa, which likely remains context-dependent and may require additional inflammatory or treatment-related triggers to clinically manifest. - Source: PubMed
Publication date: 2026/03/25
Arnold Kiranya EDebick NadiaBrognard JohnGhosh Auyon J - The interaction between and the vascular endothelium of the host plays a key role in the pathogenesis of canine angiostrongylosis. The adult stage of resides in right ventricles and pulmonary arteries of dogs and foxes and maintains close contact with the endothelium, whose activation may contribute to the hemostatic and hemorrhagic disorders observed in infected animals. However, the molecular mechanisms underlying this endothelial dysfunction remain poorly understood. To investigate this interaction, an in vitro model of vascular endothelial cells was stimulated with the adult homogenate. Quantitative proteomic analysis, combined with bioinformatic tools, identified 691 and 6011 protein groups in the cell supernatants and the cell lysates, respectively. Of these, 213 proteins in the cell supernatants (193 up-regulated and 20 down-regulated) and 564 in the cell lysates (358 up-regulated and 206 down-regulated) showed differential expression compared to control cells. Up-regulated proteins included TFPI, CD59, VWF, ANGPT2, MMRN1, and FLT1, which are involved in endothelial activation, angio-genesis, and coagulation regulation. Conversely, C3, SERPINE1, SERPINB2, PLAU, PLAUR, and ICAM1 were down-regulated, suggesting modulation of fibrinolysis, inflammation, and cell adhesion pathways. These findings indicate that adult homogenate induces a multifactorial endothelial activation characterized by dysregulation of coagulation, complement, and vascular remodelling pathways. Future studies focusing on the temporal and molecular characterization of endothelial responses to excretory/secretory antigens in both definitive and accidental hosts will further clarify the mechanisms of vascular pathology and parasite tolerance. - Source: PubMed
Publication date: 2026/03/15
Collado-Cuadrado ManuelRodríguez-Escolar IvánBalmori-de la Puente AlfonsoMontero-Calle AnaVázquez-Ávila SaraMacchioni FabioBarderas RodrigoSotillo JavierPericacho MiguelMorchón Rodrigo - Neuro-immune interactions are critical in cancer, yet their molecular features in bladder cancer remain unclear. We analyzed transcriptomic data from TCGA and UCSC Xena to investigate the expression profiles and molecular subtypes of neuro-immune-related genes, and constructed a neuro-immune-related score (NAS) model. Single-cell transcriptomic data were integrated to explore the immune microenvironmental features, and functional validation was performed by knocking down SERPINE2 with shRNA in T24 cells. The results showed that six core genes (SERPINE2, NXPH4, SERPINB2, C2orf40, SERPINB12, SERPINB10) were identified to stratify patients into high- and low-risk groups, with robust predictive power across clinical subgroups and validation cohorts. Single-cell RNA-seq data revealed significant NAS heterogeneity among cell populations. The NAS-high state was enriched in TGFβ, EGF, and FGF signaling with activation of EZH2 and SMARCA4, while the NAS-low state showed immune-regulatory features. Functional assays confirmed that SERPINE2 knockdown suppressed proliferation, migration, invasion, while increasing apoptosis of T24 cells, highlighting its oncogenic role. Moreover, genome-wide association studies (GWAS) suggested that genetic variants in SERPINE2 and related genes may increase bladder cancer susceptibility. Collectively, our findings provide novel insights into neuro-immune-driven tumor heterogeneity and immune remodeling, establish the NAS model as an innovative prognostic tool, and identify SERPINE2 as a promising therapeutic target for precision management of bladder cancer. - Source: PubMed
Publication date: 2026/03/04
Nie QiweiJiang MinyaoWan SongXi MingHua WeiJiang FunengZhong Weide