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
- Diseases of the central nervous system (CNS) often include neuronal damage. This study examined proteins crucial to apoptosis and neuronal signalling for identifying causes of neuronal dysfunction in two animal models: Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) and ethidium bromide (EtBr)-induced focal spinal cord injury. Transcriptomic analysis revealed increased levels of pro-apoptotic molecules including Caspase 8 (Casp8) and Cathepsin B (CTSB), but no significant changes in synaptic proteins including synaptophysin, synaptosomal-associated protein of 25 kDa (SNAP25) and postsynaptic density protein of 95 kDa (PSD95). Immunohistochemistry showed increased levels of pro-apoptotic proteins Casp8 and CTSB in the grey matter of TMEV-IDD but reduced levels of these proteins following EtBr injection. Synaptophysin, a marker for neuronal signalling, was reduced in the grey matter in both models. Drebrin, a protein related to neuronal plasticity, was significantly reduced in the grey matter of EtBr-injected mice, but increased in the white matter of TMEV-infected mice. Summarized, the upregulation of pro-apoptotic molecules in TMEV-IDD without apoptotic neurons suggests an incomplete apoptosis, while their reduction in EtBr-injected mice may indicate a reversible neuronal damage. The reduction of synaptophysin in both models indicates a possible impairment of synaptic transmission while the reduction of Drebrin in EtBr-injected mice may be associated with a reduced synaptic plasticity. - Source: PubMed
Publication date: 2026/04/22
Dembowski MartinBurigk LauraBaumgärtner WolfgangHansmann Florian - We previously reported that germline complement deletion protected cognition and hippocampal synapses in aged APP/PS1dE9 mice despite increased amyloid plaques. To assess whether global C3 lowering in adult amyloid mice might be neuroprotective, we crossed our C3 inducible conditional mice with knockin mice. - Source: PubMed
Publication date: 2025/12/20
Singh BrijendraBatista Andre FSpooner Emma TColletti Brianna RSaido Takaomi CCarroll Michael CLemere Cynthia A - The purpose of our study was to assess if spinacetin (SPC), a flavonoid found in spinach, can alleviate the cyclophosphamide (CYP)-induced changes in cystometric and inflammatory parameters indicative of the development of hemorrhagic cystitis. The animal experiments were conducted in female Wistar rats. The cohort of 60 animals was grouped as follows: I-control, II-CYP group, III-SPC group, and IV-CYP + SPC group. The cystometry and biochemical analyses were performed after a fortnight of SPC administration. SPC was found to restore normal cystometric parameters in CYP-induced cystitis and, similarly, it normalized c-Fos expression changes in the central micturition regions. SPC further prevented a massive increase in the bladder wall thickness/permeability due to exposition to CYP administration. CYP instillation resulted in the elevation of biomarkers found in urine (brain-derived neurotrophic factor, BDNF, and nerve growth factor, NGF), and in the bladder detrusor muscle (Rho kinase and vesicular acetylcholine transporter, VAChT), which were successfully restored after administration of SPC. As for the biomarkers in the bladder urothelium, the CYP-induced increases in TNF-α, IL-1β, IL-6, calcitonin gene-related peptide (CGRP), malondialdehyde, 3-nitrotyrosine, insulin-like growth factor-binding protein 3 (IGFBP-3), occludin, organic cation transporter 3 (OCT-3), orosomucoid-1 (ORM1), pituitary adenylate cyclase receptor 1 (PAC1), synaptosomal-associated protein 23 (SNAP23), SNAP25, and synaptic vesicle glycoprotein (SV2A) levels were attenuated by SPC. Finally, CYP administration resulted in a decrease in the heparin-binding EGF-like growth factor (HB-EGF), hemopexin (HPX), T-H protein, and tight junction protein (Z01), and we noted the successful restoration of all these changes in concentrations after application of SPC. In summary, SPC robustly mitigated cyclophosphamide (CYP)-induced cystometric dysfunction and biochemical alterations characteristic of iatrogenic hemorrhagic cystitis. These findings position SPC as a compelling therapeutic candidate and warrant further translational investigation for the management of CYP-induced bladder injury. - Source: PubMed
Publication date: 2026/03/27
Wróbel JanZapała ŁukaszNiemczyk GrzegorzBogaczyk AnnaKluz TomaszWdowiak ArturMisiek AleksandraBojar IwonaPoleszak EwaMisiek MarcinGaweł KingaWróbel Andrzej - Botulinum neurotoxins (BoNTs) are the most potent biological toxins known and widely used as biopharmaceuticals. Yet pharmaceutical potency testing still relies largely on the mouse bioassay, raising ethical concerns and conflicting with 3 R principles. Sensitive, serotype‑independent human cell‑based alternatives are particularly needed for the emerging serotypes BoNT/E and BoNT/F, for which no validated in vitro potency assay currently has been reported. In this study, human iPSC‑derived motor neurons were generated, cryopreserved as motor neuron progenitors, matured to day 30, and exposed to serial dilutions of BoNT/E or BoNT/F. Toxin activity was quantified via Western blot detection of SNAP25 (BoNT/E) using a full-length antibody, whereas for VAMP2 (BoNT/F), both full-length and neoepitope-specific antibodies were used to quantify substrate cleavage. IC₅₀ values were calculated by non‑linear regression and converted to LD₅₀/mL equivalents for comparison with mouse bioassay data. Measured IC₅₀ values were 0.769 pM for BoNT/E and 0.802 pM (full‑length) or 7.645 pM (neoepitope) for BoNT/F, corresponding to 4.54 LD₅₀/mL for BoNT/E and 2.46 LD₅₀/mL (full‑length) for BoNT/F, closely matching mouse bioassay potencies. Combining these data with prior results for BoNT/A and BoNT/B demonstrates a potency order: BoNT/A ≫ BoNT/B ≈ BoNT/F ≈ BoNT/E. These results confirm human iPSC‑derived motor neurons as a sensitive, physiologically relevant model capable of detecting four medically important BoNT serotypes. While Western blotting provides robust determination of potency, this cellular model well suited for adaptation to serotype-independent high‑throughput formats, paving the way for animal‑free BoNT potency testing. - Source: PubMed
Publication date: 2026/04/08
Schenke MarenWestphal AliceWeisemann JasminRummel AndreasDorner Brigitte GKlawonn FrankSeeger Bettina - Cognitive dysfunction in multiple sclerosis (MS) has gained increasing attention over recent decades, reflecting its substantial effects on day-to-day functioning and the limited availability of targeted therapies. This review addresses contemporary advances in the role of cognition to detect disease progression, examines biological and MRI correlates of cognitive dysfunction, and summarizes the evidence for treatment effects. - Source: PubMed
Publication date: 2026/04/06
De Meo ErmelindaPortaccio EmilioAmato Maria Pia