Ask about this productRelated genes to: SERPINB10 antibody
- Gene:
- SERPINB10 NIH gene
- Name:
- serpin family B member 10
- Previous symbol:
- PI10
- Synonyms:
- bomapin
- Chromosome:
- 18q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-13
- Date modifiied:
- 2016-04-06
Related products to: SERPINB10 antibody
Related articles to: SERPINB10 antibody
- 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 - A subset of severe asthma is characterized by neutrophilic airway inflammation in which epithelial activation of the NLRP3 inflammasome pathway is implicated. Recent reports link SERPINB10 to neutrophil activation in inflammatory disease. We hypothesized that SERPINB10 contributes to neutrophilic inflammation in asthma. Since viral infection triggers airway neutrophilia in asthma, we sensitized mice with house dust mite (HDM) and challenged them with HDM and poly(I:C), a viral double-stranded RNA analog. Compared to wild-type mice, mice exhibited reduced neutrophil counts in bronchoalveolar lavage cells and alleviated inflammatory cell infiltration around airways. Expression of inflammatory cytokines such as Il-1β and Il-6 was also decreased in lung tissues from mice. In cultured HBE cells, knockdown decreased IκBα phosphorylation and suppressed poly(I:C)-induced expression of IL-1β and IL-6. Moreover, the expression of NLRP3 and pro-IL-1β in lung tissues of mice was decreased. Conversely, overexpression enhanced IL-1β and IL-6 expression in HBE cells, which was blocked by either an IκBα phosphorylation inhibitor or an NLRP3 inhibitor. Of note, SERPINB10 expression in bronchial brushings from non-eosinophilic asthma patients was enhanced and significantly correlated with the severity of airflow limitation, and the expression of NLRP3, IL-1β, and IL-6. Altogether, SERPINB10 promotes IL-1β and IL-6 expression by upregulating NF-κB and NLRP3 signaling in airway epithelial cells, thereby driving neutrophilic airway inflammation in asthma. SERPINB10 is a potential therapeutic target for airway neutrophilia in asthma. - Source: PubMed
Publication date: 2025/10/10
Kong WeiqiangHuang ChunliZhao LuChen GongqiGu WeiJie HuiruWang ZhenXiong TiantianYi LinglingFeng YuchenZhen Guohua - Macrophage M2 polarization plays a critical role in type 2 airway inflammation in asthma. We previously reported that serine peptidase inhibitor, clade B, member 10 (SERPINB10) promotes airway eosinophilic inflammation in asthma. - Source: PubMed
Publication date: 2025/05/10
Zhao LuWu WenliangChen GongqiHuang ChunliKong WeiqiangGu WeiJie HuiruYi LinglingZhen Guohua - The effects of inhaled corticosteroids (ICS) on healthy airways are poorly defined. - Source: PubMed
Publication date: 2024/04/30
Marchi EmanueleHinks Timothy S CRichardson MatthewKhalfaoui LatifaSymon Fiona ARajasekar PoojithaClifford RachelHargadon BeverleyAustin Cary DMacIsaac Julia LKobor Michael SSiddiqui SalmanMar Jordan SArron Joseph RChoy David FBradding Peter - Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by the production of autoantibodies, immune complex deposition, and tissue/organ damage. In this study, we aimed to identify molecular features and signaling pathways associated with SLE severity using RNA sequencing (RNA-seq), single-cell RNA sequencing (scRNA-seq), and clinical parameters. We analyzed transcriptome profiles of 45 SLE patients, grouped into mild (mSLE, SLEDAI ≤ 9) and severe (sSLE, SLEDAI > 9) based on SLE Disease Activity Index (SLEDAI) scores. We also collected clinical data on anti-dsDNA, ANA, ESR, CRP, snRNP, AHA, and anti-Smith antibody status for each patient. By comparing gene expression across groups, we identified 12 differentially expressed genes (DEGs), including 7 upregulated (CEACAM6, UCHL1, ARFGEF3, AMPH, SERPINB10, TACSTD2, and OTX1) and 5 downregulated (SORBS2, TRIM64B, SORCS3, DRAXIN, and PCDHGA10) DEGs in sSLE compared to mSLE. Furthermore, using the CIBERSORT algorithm, we found that Treg cells were significantly decreased in sSLE and negatively correlated with AMPH expression, which was mainly expressed in Treg cells from SLE patients according to public scRNA-seq data (GSE135779). Overall, our findings shed light on the molecular mechanisms underlying SLE severity and provide insight into potential therapeutic targets. - Source: PubMed
Publication date: 2023/07/24
Zhang XiaojingZhang JialiPan ZhaobingZhang YuxiXu XiaoqingSheng YujunZhu ZhengweiZhou FushengWen Leilei