SPINT1 Antibody
- Known as:
- SPINT1 Antibody
- Catalog number:
- GWB-MV531I
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- SPINT1 Antibody
Related genes to: SPINT1 Antibody
- Gene:
- SPINT1 NIH gene
- Name:
- serine peptidase inhibitor, Kunitz type 1
- Previous symbol:
- -
- Synonyms:
- HAI, MANSC2
- Chromosome:
- 15q15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-18
- Date modifiied:
- 2016-10-05
Related products to: SPINT1 Antibody
Related articles to: SPINT1 Antibody
- Background Comorbidity between schizophrenia (SCZ) and chronic diseases is well documented. However, it remains unknown whether unaffected individuals with elevated SCZ genetic liability also face increased risk, and what biological pathways may underlie these associations. Methods We analyzed 426,237 UK Biobank participants without SCZ to test associations between SCZ polygenic risk score (SCZ-PRS) and 24 chronic diseases using logistic regression. Multi-omics mediation analysis incorporated seven inflammatory markers, 1,463 plasma proteins, and 250 circulating metabolites to delineate intermediate pathways linking genetic liability to disease outcomes. Genetic colocalization analyses were further conducted to determine whether SCZ genetic liability and chronic diseases share common association signals at the locus level. Results Higher SCZ-PRS was associated with increased risk of asthma (OR=1.018, 95% CI 1.008-1.029), COPD (1.033, 1.017-1.050), liver disease (1.033, 1.015-1.051), peptic ulcer (1.032, 1.013-1.051), and fluid/electrolyte disorders (1.027, 1.014-1.040), while conferring reduced risk of diabetes (0.979, 0.968-0.991) and renal disease (0.978, 0.964-0.992). Multi-omics mediation revealed that these bidirectional associations were linked to immune cell activity (notably eosinophils, neutrophils, and monocytes), lipid and energy metabolism (lipoprotein composition, fatty-acid unsaturation, creatinine, lactate), and immune-regulatory proteins (e.g., HLA-E, CD1C, SPINT1). Shared genetic signals, notably at HLA and SLC39A8, reinforced these immune-metabolic pathways. Conclusions SCZ-PRS is associated with multiple chronic diseases among unaffected individuals, and these associations suggest shared biological pathways. These findings support a psycho-neuro-immune-metabolic interpretation of SCZ-related chronic physical comorbidity and a more integrated psychosomatic understanding of the shared biology linking psychiatric vulnerability with chronic physical disease. - Source: PubMed
Publication date: 2026/06/29
Wei WenmingCheng BolunHe DanQi XinHui JingniFeng JinCheng ShiqiangYang XuenaZhao BoyuePan ChuyuGou YifanWen YanLiu HuanJia YumengLiu LiZhang Feng - - Source: PubMed
Publication date: 2026/06/19
Wang JinyouZhang NingWang YanChen FanghongWang LeiWang KailunYao XiaoPan Xiaohui - Hepatocyte growth factor activator inhibitor type-1 (HAI-1) plays pivotal roles in epithelial integrity and tumour biology. Although implicated in various malignancies, its expression profile and prognostic value in bladder cancer (BC) remain incompletely defined. High levels of HAI-1 ectodomain in urine have previously been reported to be associated with poor prognosis in BC patients. This study aimed to determine the relationships between tissue and urine levels of HAI-1 and clinical outcomes in BC. This study used immunohistochemistry to measure HAI-1 expression across 770 BCs of all stages and grades. HAI-1 expression was scored on the basis of the percentage of positive cancer cells, subcellular localisation, and staining intensity. Additionally, HAI-1 () mRNA expression was compared with protein levels in tissue and urine. HAI-1 was highly expressed in low-grade, early-stage disease with strong membranous staining. Reduced overall HAI-1 expression, loss of membranous staining and increased cytoplasmic staining correlated with higher stage and grade and shorter survival. mRNA levels were positively correlated with membranous HAI-1 staining intensity (p = 0.005). Urinary levels of HAI-1 were negatively associated with the fraction of HAI-1 positive cancer cells and membranous staining intensity (p < 0.05). A positive correlation was observed between expression and urinary HAI-1 levels (p < 0.05). The Urobasal A subtype had lower urinary HAI-1 ectodomain levels than other subtypes. HAI-1 expression may serve as a biomarker of tumour differentiation and prognosis in BC. Increased ectodomain shedding into the urine, rather than increased expression, likely explains the higher urine HAI-1 levels seen in more aggressive tumours. - Source: PubMed
Publication date: 2026/04/24
Saeed Azad KTriantafyllakis PanagiotisGordon Naheema SJames Nicholas DZeegers Maurice PCheng K Kde Jong Joep JDavicioni ElaiBryan Richard TWard Douglas G - The choroid plexus (CP) has traditionally been regarded as a cerebrospinal fluid-producing structure; however, increasing evidence indicates that it functions as a dynamic regulatory interface involved in immune surveillance, metabolic homeostasis, and brain clearance. Neuroimaging studies consistently report CP enlargement across aging and diverse neurological and neuropsychiatric disorders, yet the underlying cellular mechanisms remain poorly integrated. In this review, we synthesize morphological, molecular, and imaging evidence to propose a sequential degenerative model of the CP epithelium. This model comprises: (1) regulated epithelial cell loss via apical extrusion, (2) compensatory hypertrophy of residual cells, (3) mitochondrial remodeling with oncocytic-like change, and (4) progressive blood-cerebrospinal fluid barrier dysfunction. At the molecular level, alterations in epithelial adhesion systems-particularly SPINT1-mediated protease regulation and E-cadherin-based adherens junction stability-may initiate epithelial instability. Hypertrophic epithelial cells exhibit increased mitochondrial burden, reflected by Tom20 expression, which may initially support metabolic adaptation but ultimately contribute to oxidative stress and functional decline. At the macroscopic level, the cumulative effects of cell loss, hypertrophy, and mitochondrial remodeling likely underlie CP enlargement detectable by magnetic resonance imaging. This framework positions CP enlargement as an imaging-visible manifestation of epithelial stress and provides a structural-molecular basis for interpreting CP alterations in brain aging and neurodegenerative disorders. - Source: PubMed
Publication date: 2026/03/09
Murakami RyutaUeno Masaki - Pericellular proteolysis is essential for maintaining tissue homeostasis. Central to this process are hepatocyte growth factor activator inhibitor-1 (HAI-1) and HAI-2, membrane-bound inhibitors that regulate type II transmembrane serine proteases, including matriptase and prostasin, through high-affinity Kunitz domains. This review summarizes current understanding of their molecular structures, physiological roles, and cancer-related clinical relevance. Genetic models reveal HAI-1 is critical for placental and skin development, while HAI-2 is crucial for neural tube closure and intestinal integrity. In cancer, HAIs generally act as tumor suppressors. Their downregulation, often via promoter hypermethylation, leads to excessive activation of hepatocyte growth factor/c-MET or protease-activated receptor-2/NF-κB signaling, promoting epithelial-mesenchymal transition and cancer progression. Clinically, reduced HAI levels in tumors correlate with metastasis and poor prognosis in several carcinomas. Paradoxically, elevated HAI expression in certain cancers suggests context-dependent pro-tumor functions. Emerging evidence links HAI loss to immune suppression, notably via M2 macrophage polarization in lung cancer. Finally, we highlight future directions for identifying tissue-specific serine proteases, downstream signaling, and therapeutic strategies, including recombinant mimetics and epigenetic reactivation, in precision oncology. In conclusion, HAI-1 and HAI-2 are key regulators of tissue homeostasis and cancer, with overlapping yet distinct functions, which present promising opportunities for therapeutic targeting. - Source: PubMed
Publication date: 2026/02/19
Chen Chun-YingLin Tai-NoHuang Hsiang-Po