SNAP25,1_206aa, Human, Recombinant, E.coli
- Known as:
- SNAP25,1_206aa, Human, Recombinant, E.coli
- Catalog number:
- SNP0801
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- SNAP25 1_206aa Human Recombinant .coli
Related genes to: SNAP25,1_206aa, Human, Recombinant, E.coli
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
- 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: SNAP25,1_206aa, Human, Recombinant, E.coli
Related articles to: SNAP25,1_206aa, Human, Recombinant, E.coli
- Preclinical Alzheimer's disease (AD) research requires models with age-dependent, physiologically relevant amyloid pathology, unlike overexpression in transgenic lines. We characterized the humanized knock-in model to define translationally relevant therapeutic windows. - Source: PubMed
Publication date: 2026/09/10
Sloan Lucy JGarceau Dylan TRyan Nick JPomeroy-Tuck JusticeChidambaram RiteshRagan TimPandey Ravi SBloss Erik BCarter Gregory WOblak Adrian LSasner Michael - - Source: PubMed
Publication date: 2026/09/26
Gaetani LorenzoBellomo GiovanniChiasserini DavideDe Rocker CharlotteGoossens JuliePaoletti Federico PaoliniVanmechelen EugeenParnetti Lucilla - 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