Ask about this productRelated genes to: UCHL1 antibody
- 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 antibody
Related articles to: UCHL1 antibody
- NICE head injury guidance prioritises sensitivity but results in high CT utilisation and low diagnostic yield, contributing to Emergency Department (ED) crowding, particularly among older adults after falls. GFAP/UCH-L1 blood biomarkers may support safer CT stewardship, although limited specificity in older adults may reduce clinical impact. - Source: PubMed
Publication date: 2026/04/29
O'Shea Paula MUmana EtimbukBroderick ShaneByrne EileenSamad Nadia MNnamani ChizobaBarrett SimonO'Rourke MeadhbhWalsh IanBolster FerdiaDuddy JohnLee Graham RO'Halloran Philip J - Mild traumatic brain injury (mTBI) presents diagnostic challenges, with head computed tomography (head CT) often overutilized in emergency settings. Blood biomarkers such as glial fibrillary acidic protein (GFAP) and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) have shown promise in early injury detection. Aim of this study was to evaluate the diagnostic utility of GFAP and UCH-L1 in identifying intracranial injuries early and potential reduction in unnecessary head CT scans in mTBI patients. - Source: PubMed
Publication date: 2026/02/27
Osmić-Husni AlmaJadrić RadivojJović-Lacković SvetlanaŽabić AidaČamdžić-Smajić Sabina - Gastrointestinal (GI) dysmotility is a highly prevalent and clinically significant feature of Rett syndrome (RTT), yet its underlying mechanisms remain poorly defined. Here, we investigated these mechanisms of GI dysmotility in a mouse model of RTT. First, we observed that MeCP2 was expressed in murine myenteric ganglia, including in enteric neurons and that males developed maturation-associated functional regression in their GI motility. In dysmotile mice, longitudinal muscle-myenteric plexus tissue showed marked reductions in enteric soforms and , whereas expression of the BDNF receptor isoforms TrkB.FL and TrkB.T1 was not significantly altered, consistent with reduced enteric BDNF-TrkB signaling. Despite impaired GI motility, mice showed no significant changes in total enteric neuronal density, nitrergic neuronal abundance, or expression of , and In contrast, expression was significantly reduced, while expression of VIP receptor genes: and was increased, indicating disrupted VIPergic signaling. Integration with publicly available enteric single-cell/nucleus datasets and targeted qRT-PCR further suggested altered inhibitory neuronal subtype composition, with reduced signatures and increased expression, suggesting that MeCP2 loss differentially affects distinct inhibitory neuronal subpopulations. Finally, conditional loss of TrkB.FL in neural crest-derived cells reduced expression without recapitulating the full VIPergic phenotype, indicating that impaired BDNF-TrkB signaling contributes to, but does not completely explain, the GI dysmotility in this model of RTT. Together, these findings identify enteric BDNF-TrkB and VIPergic dysfunction as key mechanisms underlying GI dysmotility in RTT. - Source: PubMed
Publication date: 2026/04/15
Puttapaka Srinivas NAdmasu Israel AScott AinsleighSonmez GamzeSeika PhilippaRajkumar MahalakshmiValencia XavierConsorti AlanHong Su MinSlosberg JaredFagiolini MichelaKulkarni Subhash - Prior investigations of how lifetime blast exposure relates to blood biomarkers of brain injury have been limited by small sample sizes and have produced conflicting results. This investigation examined how lifetime blast exposure relates to glial fibrillary acidic protein (GFAP), ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), neurofilament light (NfL), tau, and hyperphosphorylated tau (p-tau) in service members and veterans (SMVs) with and without uncomplicated mild TBI (mTBI). Participants were 422 SMVs prospectively enrolled in a Defense and Veterans Brain Injury Center-Traumatic Brain Injury Center of Excellence Longitudinal TBI Study. Participants were divided into four groups based on self-reported lifetime blast exposure history as assessed by a single question: none ( = 93), low ( = 136), medium ( = 71), and high ( = 122). Analysis of Covariance was used to examine group differences on GFAP, UCH-L1, NfL, tau, and p-tau. There was a significant effect of blast exposure group on NfL ( = 0.002, η = 0.034) and GFAP ( = 0.035, η = 0.021), but not UCH-L1, tau, or p-tau. comparisons with Bonferroni correction indicated NfL was higher in the No Blast group compared with the Low Blast ( = 0.004) group, but not the Medium Blast ( = 0.069) or High Blast ( = 1.0) groups. GFAP did not significantly differ between the groups after Bonferroni correction (ps > 0.05). Overall, the lone finding that survived correction for multiple comparisons suggested that participants with low levels of self-reported blast exposure exhibited lower levels of NfL than participants with no history of blast exposure. There were no differences in UCH-L1, tau, or p-tau based on self-reported blast exposure in a large sample of SMVs with and without mTBI. - Source: PubMed
Publication date: 2026/04/24
Lippa Sara MarieGill JessicaLai ChenKennedy JanHungerford LarsBailie Jason MBrickell TraceyFrench LouisLange Rael - The G protein-coupled receptor 68 (GPR68) detects variations in extracellular pH, and has potential roles in homeostasis and responses to ischaemia and inflammation within different organs, including the gastrointestinal tract. However, in the human colon the distribution of GPR68 remains unclear. We examined the localization and density of GPR68 within the ascending (AC) and descending (DC) human colon from younger and older adults. - Source: PubMed
Publication date: 2026/04/07
Baidoo NicholasRasis Enrica DePaine LukeBulmer David CSanger Gareth J