Ask about this productRelated genes to: SNAP25 antibody
- Gene:
- SNAP25 NIH gene
- Name:
- synaptosome associated protein 25
- Previous symbol:
- SNAP
- Synonyms:
- SNAP-25, RIC-4, RIC4, SEC9, bA416N4.2, dJ1068F16.2
- Chromosome:
- 20p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-24
- Date modifiied:
- 2016-10-05
Related products to: SNAP25 antibody
Related articles to: SNAP25 antibody
- Rabies virus causes fatal neurological disease, but the mechanisms by which its glycoprotein G influences neuronal dysfunction remain incompletely understood. In this study, we rescued two recombinant RABV LBNSE strains carrying G proteins from either the attenuated SAD-B19 strain or the virulent CVS11 strain, designated as rLBNSE-SfG and rLBNSE-CfG, respectively. Infection of primary mouse neurons and challenge experiments in mice showed that rLBNSE-CfG was associated with increased early neuronal infectivity and greater neurovirulence after intracerebral (i.c.) injection. Western blot analysis revealed that the SAD-B19-derived G protein exhibited a higher apparent molecular weight than the CVS11-derived G protein. Bioinformatic analysis identified strain-specific differences in putative post-translational modification sites, which may contribute to the observed migration difference. Quantitative proteomic analysis of mouse brain tissue showed that proteins downregulated in the rLBNSE-CfG group were enriched in synaptic vesicle cycle-related pathways and synapse-associated Gene Ontology (GO) terms. Integrated analysis identified a SNARE-associated module containing Snap25, Stx1a, and Vamp2, among which Vamp2 was significantly reduced in the rLBNSE-CfG group. In primary neurons, reduced Vamp2 abundance was associated with the extracellular domain of CVS11 G protein. These findings associate CVS11-derived G protein variation with reduced Vamp2 abundance and a presynaptic vesicle-related proteomic signature, although whether these molecular alterations directly impair synaptic vesicle release remains to be determined. - Source: PubMed
Publication date: 2026/09/07
Liu ChunyuGuo HaoYin KunSun YumingMa ZipengWang FengxueNiu YanWen Yongjun - Pharmacodynamic models of botulinum toxin type A map a mean concentration onto a smooth dose-response curve, yet the outcome is binary and arises from a finite population of near-threshold motor units. We analyse a discrete model in which units are silenced once local SNAP-25 cleavage exceeds a unit-specific threshold, and a functional block of neuromuscular transmission follows once the silenced fraction exceeds a collective threshold. Whether that collective threshold is a fraction of the population or a fixed count changes the location of the dose-response curve and not its steepness: under a fraction, potency is invariant to unit number at fixed dose-concentration gain, and the transition contracts in absolute dose where fixed-count architectures require it to widen. The width contracts as N-1/2, an exponent that is prior and not claimed here. One consequence needs no measurement: a quantal terminal response caps the silenced fraction below unity, so any fixed count fails above a target size it determines, whereas the toxin block targets differ by orders of magnitude. A second reinterprets existing data, flat cohort dose-response curves being what a near-step individual response predicts once convolved with between-subject dispersion. Outcome is accordingly less repeatable in the smallest targets. No parameter is fitted. - Source: PubMed
Publication date: 2026/09/21
Armenti Andrea FeliceArmenti Francesco - 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 - To elucidate the Δ⁹-tetrahydrocannabinol (THC)-like discriminative stimulus effects of 4F-ABUTINACA and to investigate the potential mechanisms underlying anxiety-like behaviors induced by chronic 4F-ABUTINACA administration. - Source: PubMed
Publication date: 2026/09/21
Shi BaobaoWang HaitaoZhou WenhuaLai Miaojun - Spatial long-read technologies are increasingly common but usually lack single-cell resolution. This leaves unanswered whether spatially variable isoforms reflect variability within one cell type or differences in region-specific cell-type composition. Here, we developed Spl-ISO-Seq2 (500-nm resolution) and accompanying software, Spl-IsoQuant-2 and Spl-IsoFind, enabling long-read sequencing of >450 million barcodes versus 80,000 previously. Applying this to the adult mouse brain, we compared differential isoform abundance between known regions and spatial isoform patterns independent of predefined regions. Both identified overlapping hits, for example, Rps24 in oligodendrocytes. For known Snap25 spatial isoform variation, we show that it occurs in excitatory neurons. The region-agnostic approach also uncovered patterns missed by region-based comparisons, for example, for Ighm. Notably, many spatial isoform signals are not driven by cell-type composition alone. Finally, our software is applicable to many spatial and single-cell protocols, demonstrating reproducibility between platforms (for example, Visium HD/Stereo-seq). Overall, our experimental/analytical methods enable a submicron-resolution-isoform view and open avenues for spatial isoform disease research. - Source: PubMed
Publication date: 2026/09/04
Michielsen LiekePrjibelski Andrey DFoord CareenSpiegelman YelizavetaKim TaewooHu WenJarroux JulienHsu JustinePfeil RebeccaZhang XinyiGan LiTomescu Alexandru IHajirasouliha ImanTilgner Hagen U