UCHL1 Mouse-Mono
- Known as:
- UCHL1 Mouse-Mono
- Catalog number:
- 422721F
- Product Quantity:
- 6ml
- Category:
- -
- Supplier:
- Nichereion
- Gene target:
- UCHL1 Mouse-Mono
Related genes to: UCHL1 Mouse-Mono
- Gene:
- UCHL1 NIH gene
- Name:
- ubiquitin C-terminal hydrolase L1
- Previous symbol:
- PARK5
- Synonyms:
- PGP9.5, Uch-L1
- Chromosome:
- 4p13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-15
- Date modifiied:
- 2015-11-13
Related products to: UCHL1 Mouse-Mono
Related articles to: UCHL1 Mouse-Mono
- Traumatic brain injury (TBI) is a leading cause of acquired epilepsy, death, and long-term disability, yet reliable biomarkers to predict chronic sequelae such as post-traumatic epilepsy (PTE) remain limited. We evaluated the associations between circulating blood biomarkers of neuronal, glial, and synaptic injury and the subsequent development of PTE. - Source: PubMed
Publication date: 2026/09/22
Calió Michele LongoniForesti Maira LiciaSantos Luis EduardoMosini Amanda CristinaSilva Clivandir SeverinoPompeu ClaraWillers JulianaCalvo Thyago Lealde Andrade Almir Ferreirada Silva Saul AlmeidaGarzon ElianaMello Luiz Eugênio - Neurodegenerative diseases represent a growing global health burden, largely driven by population ageing and the absence of disease-modifying therapies. Current treatment strategies remain largely symptomatic, highlighting the need for the identification of novel neuroprotective agents targeting key pathological mechanisms such as impaired proteostasis and dysregulated signalling pathways. In this study, an integrated in silico workflow was employed to investigate LC-MS-annotated metabolites from (avocado) seed extract for their binding interactions with two neurodegeneration-related protein targets, GPR52 and UCHL1. Untargeted LC-MS profiling was followed by metabolite annotation, target prediction, molecular docking, molecular dynamics (MD) simulations (50 ns for GPR52 and 100 ns for UCHL1), and binding free energy calculations using MM/GBSA and MM/PBSA approaches. Among LC-MS-putatively identified metabolites, moupinamide and echitoserpidine showed stable binding across molecular dynamics simulations, supported by consistent structural stability and favourable binding free energies against GPR52 and UCHL1 respectively. In contrast, scoulerine and piperine exhibited less favourable MM/PBSA binding free energies despite their moderate docking scores, indicating weaker predicted binding affinity. ADMET analysis revealed generally acceptable drug-like properties, but limitations in pharmacokinetics and central nervous system accessibility, particularly blood-brain barrier permeability, cardiotoxicity and metabolic stability. Overall, the results suggest that LC-MS-annotated metabolites from seed extract may represent potential candidates for further investigation as modulators of GPR52 and UCHL1, with moupinamide and echitoserpidine emerging as the most promising scaffolds among the evaluated metabolites based on integrated docking, molecular dynamics, and binding free-energy analyses. However, further structural optimization and experimental validation are required to confirm their biological relevance and assess their suitability for neurodegeneration-related drug discovery. - Source: PubMed
Publication date: 2026/09/19
Salami YusufOlasore Holiness Stephen AdedejiEbuehi Osaretin Albert Taiwo - Multiple sclerosis (MS) is a neurodegenerative and inflammatory disease affecting gray and white matter in the brain. Due to the highly variable presentation of MS, making a reliable long-term diagnosis based solely on initial clinical findings is extremely challenging. Long noncoding RNAs (lncRNAs) have been shown in recent research to have a role as prospective biomarkers that may offer data to forecast the onset and course of disease. - Source: PubMed
Publication date: 2026/09/19
Rajabi AliGross Jeffrey DSamadi Ali - Parkinson's disease (PD) is a progressive neurodegenerative disorder primarily affecting dopaminergic neurons in the mesencephalon. With rising global incidence, especially in individuals over 60, PD presents with motor and non-motor symptoms. While monogenic forms account for a subset of cases, genetic heterogeneity and variable expressivity complicate diagnosis and management. This study aimed to evaluate the genetic profile of a Turkish PD cohort through clinical exome sequencing (CES), assess genotype-phenotype correlations, and identify structural rearrangements. A retrospective analysis was conducted on 137 patients diagnosed with Parkinson's disease according to the Movement Disorder Society (MDS) clinical diagnostic criteria. Targeted next-generation sequencing (NGS) analysis was performed, and identified genetic variants were strictly classified in accordance with the American College of Medical Genetics and Genomics (ACMG) guidelines and current gene-disease validity consensus. Copy number variations (CNVs) were assessed utilizing NGS read-depth algorithms. Following rigorous evaluation according to ACMG criteria and current gene-disease validity consensus, definitive disease-causing variants explaining the PD phenotype were identified in 10 patients (7.30%). This definitive diagnostic yield was driven entirely by established PD loci: GBA1 (9 patients) and a homozygous deletion in PRKN (1 patient). Beyond this definitive group, several notable variants in OMIM-associated PD genes (including LRRK2, FBXO7, PARK7, and EIF4G1) were characterized as VUS or susceptibility findings, displaying strong clinical correlations with progressive motor and complex phenotypes. A monoallelic PINK1 variant and findings in GIGYF2 and UCHL1 were strictly excluded from the causal diagnostic yield. A novel heterozygous duplication involving LRRK2 exons 6-20 was also identified; however, as it likely results in a loss of function, its pathogenicity remains uncertain under dominant gain-of-function models. Clinical exome sequencing effectively delineates the complex genetic landscape of PD in the Turkish population. While the definitive diagnostic rate is 7.30% under strict causal criteria, the characterization of prominent VUS in OMIM-associated genes and a novel LRRK2 structural variant undetected by routine MLPA highlights the evolving complexity of PD genetics and the critical need for integrating comprehensive, read-depth-based CNV analysis into standard pipelines. - Source: PubMed
Publication date: 2026/09/19
Canbek SezinGulseven M FatihMert GoncagulSenol M Guney - Redox stress is a significant contributor to the molecular dysfunction associated with traumatic brain injury (TBI). Each of the canonical molecular biomarkers of TBI, including GFAP and UCHL1, demonstrate a clear relationship with redox stress via protein oxidation and enzymatic inhibition. Additionally, several markers of redox stress have demonstrated utility in assessing preclinical and clinical TBI, including F2-isoprostanes, generated from the oxidation of arachidonic acid. Thus, we investigated the role of urinary 8-isoprostane as a biomarker for delineating between sham and impacted mice. In this study, male and female mice (n = 19) subjected to five daily impacts using a repeated impact acceleration (rIA) model were evaluated against sham mice for neurological deficits. Impacted mice exhibited behavioral deficits, with increases in righting reflex (RR) times (p < 0.0001), and time-course increases in modified neurological severity scores (mNSS) (p < 0.01). Urine collected immediately following (day 5) and 72 h post-rIA (day 8) revealed time-course increases in 8-isoprostane levels (p < 0.05). Tissue-based protein expression for several markers of molecular dysfunction was assessed using immunoblotting in a two stage discovery based strategy, for which GFAP expression significantly differed with respect to treatment (p < 0.0001) and sex (p < 0.01). Pooled, unadjusted analysis identified a significant relationship between GFAP and urinary 8-isoprostane levels at day 8 (R = 0.75; p < 0.0001) with a non-significant, attenuated within-group relationship (R = 0.08; p > 0.05). Overall, these results suggest repeated impacts using a preclinical TBI mouse model induce acute neurobehavioral deficits, assessed via RR and mNSS, and molecular deficits, including increases in GFAP and urinary 8-isoprostane. - Source: PubMed
Publication date: 2026/09/19
McDonald Brandon ZGee Connor CTarudji Aria WCurtis Evan TKievit Forrest M