SNAP25 Antibody
- Known as:
- SNAP25 Antibody
- Catalog number:
- 32111
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- SNAP25 Antibody
Related 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
- 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 - Botulinum toxin type A (BoNT-A) is increasingly recognized for tissue-level effects beyond neuromuscular blockade, but its impact on dermal collagen composition remains incompletely characterized. Acetyl hexapeptide-8 (Argireline) is a SNAP-25 mimetic cosmeceutical peptide whose biological activity at the tissue level is unclear. This study evaluated the effects of BoNT-A, Argireline, and their combination on dermal collagen type I/III and Substance P (SP) expression in a flap model. - Source: PubMed
Publication date: 2026/08/31
Acuner BurçinGörgülü TahsinIşıktekin EmrahKaymaz Morkoç EsinKargı Ahmet Eksal - Synaptic vesicle fusion is orchestrated by the soluble N-ethylmaleimide-sensitive factor attachment receptor (SNARE) complex. The SNARE complex includes SNAP25, synaptobrevin-2, and syntaxin-1. This machinery drives action potential-evoked release, as well as the majority of spontaneous release. Mutations in components of the SNARE machinery can differentially affect spontaneous or evoked release and result in severe neurodevelopmental phenotypes, as exemplified by SNAP25 encephalopathies that arise from mutations in the SNAP25 gene. Among various pathogenic SNAP25 variants, L50S, V48F, and D166Y increase spontaneous glutamate release that destabilizes network activity. Patients who carry these variants develop recurrent seizures that are refractory to conventional antiepileptic drugs, which primarily act on components of evoked neurotransmission and leave spontaneous release abnormalities unaddressed. To surmount this limitation, we explored a strategy targeting homeostatic plasticity mechanisms with lithium, which has been shown to downscale postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR). In vitro, lithium corrected cellular phenotypes in neurons expressing SNAP25 variants. In vivo, we generated a knock-in mouse model recapitulating the SNAP25 L50S mutation to test these results. These mice displayed increased neonatal mortality, infertility, hypomobility, frequent seizure activity, anxiety-like behavior, social deficits, and impaired learning and memory. Chronic lithium treatment reduced seizure frequency and ameliorated long-term memory and locomotor activity. Taken together, lithium alleviated synaptic and behavioral disturbances driven by pathological spontaneous glutamate release by inducing homeostatic AMPAR downscaling. Thus, this work provides a mechanistically grounded therapeutic strategy for SNAP25 encephalopathies and other disorders characterized by elevated spontaneous glutamate release. - Source: PubMed
Publication date: 2026/08/27
Uzay BurakMa Z ZackUzay Ihsan AlpAlten BarisMonteggia Lisa MKavalali Ege T