Urinary trypsin inhibitor fragment (UTI)
- Known as:
- Urinary trypsin suppressor fragment (UTI)
- Catalog number:
- UB0981
- Product Quantity:
- 100MG
- Category:
- -
- Supplier:
- BioBasic
- Gene target:
- Urinary trypsin inhibitor fragment (UTI)
Related genes to: Urinary trypsin inhibitor fragment (UTI)
- Gene:
- AMBP NIH gene
- Name:
- alpha-1-microglobulin/bikunin precursor
- Previous symbol:
- ITI, ITIL
- Synonyms:
- UTI, HCP, EDC1, HI30, IATIL, ITILC
- Chromosome:
- 9q32
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- SERPINA1 NIH gene
- Name:
- serpin family A member 1
- Previous symbol:
- PI
- Synonyms:
- AAT, A1A, PI1, alpha-1-antitrypsin, A1AT, alpha1AT
- Chromosome:
- 14q32.13
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: Urinary trypsin inhibitor fragment (UTI)
Related articles to: Urinary trypsin inhibitor fragment (UTI)
- Alpha-1 antitrypsin (AAT) is a serine protease inhibitor that protects tissue from neutrophil elastase and other proteases, particularly in the lung. Mutations in SERPINA1, including the Z mutation, lead to AAT deficiency (AATD), characterized by reduced circulating AAT and increased risk of pulmonary emphysema, liver cirrhosis, and hepatocellular carcinoma. Beyond these well-characterized manifestations, AATD has been associated with panniculitis, rheumatoid arthritis, and glomerulonephritis. Emerging evidence has also suggested a link between AATD and inflammatory bowel diseases (IBDs), although experimental validation is lacking. In this study, we demonstrate that PiZ transgenic mice expressing the polymer-forming ATZ display increased susceptibility to dextran sodium sulfate (DSS)-induced colitis, accompanied by marked Paneth cell abnormalities. The accumulation of polymeric ATZ in Paneth cells is associated with the endoplasmic reticulum (ER) stress response, impaired lysosomal clearance, altered association of Lysozyme-1 (Lyz1) with LC3-containing compartments, and increased Lyz1 secretion. These intestinal alterations were accompanied by changes in microbiota composition, whereas DSS exposure and exogenous lysozyme administration were associated with aggravated intestinal and hepatic pathology. Pharmacological inhibition of ER stress restored crypt homeostasis and normalized Lyz1 secretion. Human Pi*ZZ iPSC-derived intestinal organoids similarly showed ATZ polymer accumulation in secretory epithelial cells and transcriptional alterations involving ER protein processing and epithelial homeostasis. In addition, polymeric ATZ was detected in ileal crypts from a single individual with AATD and intestinal disease. Together, our data reveal a Paneth cell-intrinsic ER stress mechanism linking ATZ accumulation to gut epithelial dysfunction, highlighting a previously underexplored role of the gut-liver axis in AATD. - Source: PubMed
Publication date: 2026/09/29
Annunziata FrancescoDos Santos Matos FelipeRelvini IreneLu JingFederico GiovannaD'Agostino ClaudiaSchiano ValentinaMaffia VeronicaCustode Bruno MariaRaiola GaetanoDe Marino BarbaraDe Cegli RossellaDel Prete EugenioPolishchuk ElenaAmbrosio CarmenCompare DeboraNardone GerardoNeri FrancescoPastore Nunzia - Atherosclerosis (AS) is a chronic inflammatory vascular disease characterized by immune dysregulation, metabolic disturbance, and progressive vascular remodeling. Although anoikis resistance has been extensively investigated in cancer biology, its involvement in immune-cell persistence and plaque progression in AS remains poorly understood. - Source: PubMed
Publication date: 2026/09/11
Shen QiangFan ZhengfengHou JinchengLi FeiWang YixuanLiu ZongtaoJiang ChenDong Nianguo - Appendicular lean mass (ALM), alanine aminotransferase (ALT), and type 2 diabetes (T2D) may be genetically linked. However, the ALT-related pathway and shared signals at the candidate locus remain uncertain. We used Mendelian randomization (MR) to evaluate associations among ALM, ALT, and T2D and compared candidate-locus signals across datasets. ALM represented muscle mass, not clinical sarcopenia. Using European-ancestry GWAS summary statistics, we performed six bidirectional two-sample MR analyses, multivariable MR (MVMR) with finite-sample t-based inference, and exploratory path-specific two-step MR. FinnGen R12 provided the T2D outcome data for MR and pathway analyses. Pathway analyses used 5000 shared-sampling bootstrap replicates to assess uncertainty in path estimates. We combined locus-level coloc/ABF with signal-specific SuSiE-coloc in the GRCh37 region. T2DGGI was used only for colocalization. Molecular-QTL and external-omics analyses were treated as supportive or limiting evidence. Higher genetically predicted ALM was associated with lower ALT and lower T2D risk, whereas higher genetically predicted ALT was associated with greater T2D risk. T2D→ALT was method-dependent. In MVMR, the ALT conditional effect remained positive, whereas the ALM direct effect was model-dependent. Path decomposition was compatible with an ALT-related statistical pathway, but product- and difference-based estimates disagreed, and residual heterogeneity remained. ALM-T2DGGI supported an rs28929474-related shared component, although component-cohort overlap was possible. FinnGen supported other ALT-related signals but did not independently corroborate rs28929474. Tissue eQTL and external omics did not provide consistent mechanistic support. The data support directionally connected MR-based associations and dataset-dependent shared candidate signals. These findings do not establish biological mediation, a unique causal variant, gene-level causal assignment, or a molecular mechanism. - Source: PubMed
Publication date: 2026/09/20
Wang XinyuanYang WenchuanSong ShuhuaSu HuaiyiZhang Yu - Early diagnosis of breast cancer (BC) remains challenging. The limited sensitivity and specificity of existing serum tumor markers for reliable clinical application highlight the need to develop a more accurate and efficient screening workflow. This study analyzed serum samples from 255 breast cancer patients and 300 healthy controls using matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, identifying 58 differentially expressed peptides (37 upregulated, 21 downregulated). Combined with machine learning, peptide identification, and external validation, a complete standardized workflow was established. Nine machine learning (ML) algorithms were employed and compared, including SVM, LightGBM, XGBoost, etc. The models were interpreted using SHAP and LIME to identify key features. Peptides of interest were sequenced via mass spectrometry. Their expression and potential prognostic value were further validated in breast cancer transcriptomic datasets. Nine machine learning algorithms showed favorable discriminatory ability in the study cohort. The LightGBM model achieved an AUC of 0.97 internally and maintained an AUC of 0.88, an accuracy of 0.8543, and a precision of 0.9799 externally. However, after correcting for the markedly elevated prevalence (80.3%) in the external cohort, the positive predictive value (PPV) decreased substantially under real-world screening scenarios, warranting prospective validation in true screening populations. Model interpretation and subsequent sequencing identified six core biomarker peptides: Apolipoprotein A-IV (APOA4), Serum Deprivation Response Protein (SDPR), Alpha-1-Antitrypsin (SERPINA1), Ezrin (EZR), Serglycin (SRGN), and Fibrinogen Alpha Chain (FGA). Transcriptomic corroboration suggested that these molecules were significantly dysregulated in breast cancer tissues and showed univariate prognostic associations with patient survival. These findings demonstrated the potential of a proteomics-driven integrated machine learning pipeline as a proof-of-concept auxiliary risk-stratification tool for enhancing early breast cancer diagnosis, warranting further prospective validation in real-world screening cohorts before clinical translation. - Source: PubMed
Publication date: 2026/09/07
Zhou XiaoyanLi YueDing TingLiu JialiTong DongdongMu YudongXu NanLi SipengMeng HaoGao NingHe Qian - Despite the global burden of hepatitis E virus (HEV) infection, host-virus interactions underlying HEV pathogenesis and progression to chronicity remain incompletely understood. This study aimed to characterize the host transcriptomic response to infection with HEV variants harboring different host- and virus-derived insertions in the hypervariable region (HVR), with a focus on innate immune activation. - Source: PubMed
Publication date: 2026/09/17
Schlienkamp SarahNocke Maximilian KUlrich Rainer GKinast VolkerSteinmann EikeTodt Daniel