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)
- α-Synucleinopathies are marked by persistent neuroinflammation and disabling non-motor symptoms involving nucleus accumbens (NAc) dysfunction, yet the neuroimmune mechanisms linking microglial activation to accumbal synaptic pathology remain poorly understood. Here, we identify α1-antitrypsin (AAT) as a previously unrecognized modulator of cannabinoid receptor 2 (CB2R)-associated signaling in α-syn pathology. An acute transcriptomic screen revealed prominent induction of the Serpina1 gene family, while primary-microglial and chronic AAV-α-syn experiments showed that Cnr2 deficiency amplified Serpina1/AAT responses, consistent with an insufficient compensatory reaction to persistent inflammation. Molecular docking, reciprocal co-immunoprecipitation, and surface plasmon resonance provided complementary evidence supporting an AAT-CB2R association under the respective assay conditions. Functionally, AAT reduced the α-syn-associated elevation of intracellular cAMP in an AM630-sensitive manner and attenuated ATP-evoked Ca⁺ responses, calpain-1 activity, GSK-3β N-terminal cleavage, and NLRP3/caspase-1-related cytokine production; these effects were substantially diminished in Cnr2-deficient microglia. Calpeptin reproduced key molecular effects, implicating calpain-related proteolysis in this neuroimmune response. In vivo, intracerebroventricular AAT preserved NAc synaptic ultrastructure, ameliorated excitatory synaptic abnormalities in dopamine D2 receptor-expressing medium spiny neurons, and improved fear-memory retrieval, spontaneous alternation, and anxiety-like behavior, without affecting novel object recognition or motor performance. Several effects were attenuated under Cnr2-deficient conditions, although selected electrophysiological responses persisted. Our findings identify AAT-CB2R-linked signaling as a modulator of microglial inflammatory homeostasis and support the therapeutic potential of AAT for NLRP3-associated neuroinflammation and non-motor dysfunction in α-synucleinopathies. - Source: PubMed
Publication date: 2026/09/20
Feng LinjuanLo HsuanWeng WeipinZheng JiahaoSun YixinLin WeiChen XiaochunWang YanpingPan Xiaodong - Alpha-1 Antitrypsin Deficiency (A1ATD) is associated with an increased risk of emphysema and chronic obstructive pulmonary disease (COPD). In view of the high prevalence of chronic respiratory diseases in East Tennessee and limited data on A1AT phenotypes in this area, we determined A1AT allele frequency among patients with COPD, asthma, or asthma-COPD overlap (ACO) in our clinic population. - Source: PubMed
Publication date: 2026/09/10
Dhand RajivWadi GhassanFerris JenniferOnar Gulsah SofiaTerry PaulHeidel Robert EricNemykina Yuliya - About 10% of pregnancies end prematurely before 37 weeks, without effective prevention therapies. Previously, we identified rare damaging variants in SERPINA1 encoding alpha-1-antitrypsin (AAT) in families with recurrent spontaneous preterm births and detected decreased protein and transcript levels of AAT/SERPINA1 from placentas in spontaneous preterm births. Here, we investigate genetic associations between SERPINA1 variants and gestational duration and evaluate AAT supplementation as a therapeutic intervention in a mouse model of preterm birth. SERPINA1 Pi*Z variant (rs28929474-T) is associated with gestational duration (P < 5×10) in European-ancestry mothers with spontaneous preterm and term deliveries. We detect a nine-day decrease in gestational duration and a fourfold odds for preterm birth vs. term birth in Pi*Z homozygotes (Pi*ZZ), compared to other genotypes. In transgenic mice without endogenous AAT, exogenous Prolastin treatment inhibits lipopolysaccharide induced preterm births (P < 0.05). Supplemented AAT is preferentially deposited in the placenta. Our findings support AAT's protective role in spontaneous preterm births and highlight its therapeutic potential, particularly in SERPINA1 Pi*ZZ genotype carriers. - Source: PubMed
Publication date: 2026/08/13
Koivulehto EPasanen AHaapalainen A MTiensuu HRämet MHallman M - Protein fragments are increasingly recognized as both biomarkers and therapeutic targets, offering important insights into disease mechanisms and potential intervention strategies. Evidence from in vitro and in vivo studies indicates that these fragments are not merely degradation products but possess distinct biological activities, actively modulating immune signaling and contributing to both acute and chronic inflammatory processes. Here, we provide an overview of proteases and their inhibitors, with a particular focus on peptide fragments generated through proteolytic cleavage. Special emphasis is placed on fragments derived from α1-antitrypsin (AAT), an acute-phase glycoprotein and major inhibitor of neutrophil elastase and other serine proteases. AAT-derived peptides of varying lengths, generated by both target and nontarget proteases, including metalloproteases, have been detected in human biological fluids and tissues. Beyond reflecting proteolytic activity, these peptides provide clinically relevant information on disease-associated inflammation and tissue remodeling. Accordingly, they are emerging as promising diagnostic, monitoring, and predictive biomarkers. Here, we summarize current knowledge on cleaved AAT fragments, their biological functions, and their potential clinical applications. - Source: PubMed
Börner FriedemannIwanicki TomaszHeld JuliaChorostowska-Wynimko JoannaJezela-Stanek AleksandraJanciauskiene Sabina - This study demonstrates that the long noncoding RNA (lncRNA) LINC00460 is significantly overexpressed in clear cell renal cell carcinoma (ccRCC) and is strongly associated with adverse clinical outcomes. Analysis of data from The Cancer Genome Atlas (TCGA), validated by an independent cohort (GSE53757) and quantitative real-time polymerase chain reaction (qRT-PCR), shows that high LINC00460 expression has robust diagnostic value (area under the curve [AUC] = 0.818) and predicts shorter overall survival, highlighting its potential as a prognostic biomarker. Functional enrichment analyses indicate that LINC00460 is involved in key pathways, including complement and coagulation cascades, cytokine-cytokine receptor interactions, extracellular matrix remodeling, and p53 signaling. experiments confirm that silencing LINC00460 in ccRCC cell lines (Caki-2 and ACHN) markedly inhibits tumor cell proliferation, migration, and invasion while promoting apoptosis. Mechanistically, LINC00460 knockdown reduces levels of inflammatory factors (interleukin-6 [IL-6], tumor necrosis factor-alpha [TNF-α], and C-X-C motif chemokine ligand 8 [CXCL8]) and coagulation-related proteins (C3, SERPINA1, and PLAU), and activates the p53 pathway by upregulating p21 and BAX while downregulating Bcl-2. Genomic analysis reveals higher mutation rates of and in LINC00460-high tumors, and drug repurposing screening identifies cinchonine and iproniazid as candidate therapeutic agents. These findings establish LINC00460 as an oncogenic driver in ccRCC and a promising target for both diagnosis and precision therapy. - Source: PubMed
Publication date: 2026/07/15
Dong BoLiu SongtaoWang WenyuWang Jingchun