SNAP_25 Monoclonal Antibody (SP12)
- Known as:
- SNAP_25 Monoclonal Antibody (SP12)
- Catalog number:
- ASAVAM-SV012D
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- SNAP_25 Monoclonal Antibody (SP12)
Related genes to: SNAP_25 Monoclonal Antibody (SP12)
- Gene:
- ASS1P12 NIH gene
- Name:
- argininosuccinate synthetase 1 pseudogene 12
- Previous symbol:
- ASSP12
- Synonyms:
- -
- Chromosome:
- 9p21.1
- Locus Type:
- pseudogene
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- CASP12 NIH gene
- Name:
- caspase 12 (gene/pseudogene)
- Previous symbol:
- CASP12P1
- Synonyms:
- -
- Chromosome:
- 11q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-07-25
- Date modifiied:
- 2015-08-26
- Gene:
- HYOU1 NIH gene
- Name:
- hypoxia up-regulated 1
- Previous symbol:
- -
- Synonyms:
- ORP150, HSP12A, Grp170
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-05-27
- Date modifiied:
- 2017-05-09
- Gene:
- RIDA NIH gene
- Name:
- reactive intermediate imine deaminase A homolog
- Previous symbol:
- HRSP12
- Synonyms:
- UK114, P14.5, PSP
- Chromosome:
- 8q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-03
- 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: SNAP_25 Monoclonal Antibody (SP12)
Related articles to: SNAP_25 Monoclonal Antibody (SP12)
- Delayed neurocognitive recovery (DNR) is a common postoperative complication in elderly patients, and its prevention and treatment remain challenging. Synaptosomal-associated protein 25 (SNAP-25), a potential biomarker for several neurodegenerative diseases, has been reported to be associated with the occurrence of DNR. However, whether SNAP-25 can predict the development of DNR remains unclear. Therefore, this study aimed to investigate the predictive value of preoperative SNAP-25 levels in cerebrospinal fluid (CSF) and plasma for DNR in elderly patients. - Source: PubMed
Dou Xiao-YuLi Jing-YuQiu YiXu Meng-YingDong Hai-YunXue JiaoMa Peng-LeiAn Min - Glioma recurrence and resistance to therapy remain major challenges in neuro-oncology, driven in part by profound cellular and spatial heterogeneity within the tumor microenvironment. Malignant and immune populations dynamically coexist and transition during disease progression, yet their coordinated organization remains poorly understood, and standard bulk RNA sequencing cannot resolve cell-type composition. To address these limitations, we established GliomaDeconv, a glioma-specific reference and interpretation framework for bulk RNA-seq deconvolution, derived from multi-subtype scRNA-seq datasets and implemented using established probabilistic deconvolution architecture. Application of GliomaDeconv to spatially annotated IVY GAP datasets and large bulk RNA-seq cohorts enabled systematic mapping of cellular composition, spatial organization, and dynamic evolution across glioma subtypes and disease stages. Single-cell analyses identified distinct malignant cell states, including a neural progenitor-like (NPC-like) population with strong tumor-propagating capacity, as well as multiple functionally specialized tumor-associated macrophage subsets enriched in grade- and subtype-specific patterns. GliomaDeconv-derived estimates showed biological concordance with single-cell-derived molecular programs in bulk datasets and suggested that histologically defined tumor regions are associated with distinct malignant and immune cell-state enrichments. Large-cohort analyses further identified subtype-specific cellular programs and therapy-associated phenotypic transitions. Functional validation in an orthotopic model showed that SNAP25-high/NPC-like glioma cells exhibited enhanced tumor-propagating capacity, supporting an association between this cell state and glioma progression. Collectively, GliomaDeconv bridges single-cell resolution and large-cohort transcriptomics, enabling precise dissection of glioma microenvironmental composition across subtypes and disease stages. The tool provides a practical framework for biological interpretation and is freely available at http://www.szflab.site/gliomadeconv/. - Source: PubMed
Publication date: 2026/07/07
Sun MaoyuanJiang ShanZeng YulaiLiu BeiningWang YueLi ZhenGuan YunChen JiawenZhu RuizePing WeiqiuTeng YanlinYan SonglinTang QishengFan ZhenQin ZhiyongXu HoushiShi Zhifeng - Amyotrophic lateral sclerosis is a heterogeneous and rapidly progressing neurodegenerative disorder with limited treatment options. Therefore, there is a critical need for biomarkers that capture the diverse pathophysiological mechanisms underlying disease onset and progression. Emerging evidence suggests that synaptic dysfunction is an early disease mechanism in amyotrophic lateral sclerosis. Using homebrew immunoassays, we explored a panel of pre- and post-synaptic proteins in cerebrospinal fluid of patients with amyotrophic lateral sclerosis ( = 57) and controls ( = 36). The potential value as a biomarker was explored by correlating cerebrospinal fluid levels with clinical parameters and established biomarkers for amyotrophic lateral sclerosis. Higher levels of Neurogranin (NRGN) ( = 0.003) and Vesicle-associated membrane protein 2 (VAMP2) ( = 0.014) were observed in patients with amyotrophic lateral sclerosis compared with controls. VAMP2, Synaptosome-associated protein 25 kDa (SNAP25) and β-synuclein (SNCB) correlated with individual relative disease stage, but none of the biomarkers correlated with disease progression rate. High levels of SNAP25 predicted worse survival in a univariate and stepwise multivariable analysis, but significance did not persist upon including Neurofilament light chain (NfL) levels. Synaptic proteins did not correlate with cerebrospinal fluid levels of neurofilaments or biomarkers of neuroinflammation, suggesting that they reflect different pathological mechanisms in amyotrophic lateral sclerosis. Our findings warrant further investigation to determine whether increased cerebrospinal fluid levels of synaptic proteins reflect synaptic breakdown or active release of synaptic proteins. This will help elucidate how synaptic dysfunction or damage contributes to elevated levels of synaptic markers in amyotrophic lateral sclerosis, and its underlying value as biomarker. - Source: PubMed
Publication date: 2026/06/25
Hobin FrederikDas ShreyaseeLambrechts CharlotteDe Rocker CharlotteDubin JonasOmbelet FoukeDe Vocht JokeLamaire NikitaVanmechelen EugeenPoesen KoenVan Damme Philip - Synaptic dysfunction is a central feature of many neurologic diseases, and the soluble -ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex plays a critical role in regulating synaptic vesicle fusion and neurotransmitter release. Despite the rapidly growing body of research on SNAREs, comprehensive reviews addressing their mechanisms, as well as the influence of genetic variants and epigenetic regulation, remain limited. This review aims to address this gap. Disruption of SNARE processes can impair synaptic signaling and lead to neurologic pathology. Genetic variants in SNARE-related genes, including VAMP2, STX1A/STX1B, SNAP-25, STXBP1, UNC13A, SYT1, RIM, and RAB3, have been associated with a broad spectrum of neurologic conditions. In addition to genetic variants, emerging evidence indicates that epigenetic mechanisms can regulate the function of SNARE-related genes in physiologic processes and contribute to disease pathogenesis. Genetic variants are increasingly used as diagnostic markers and may inform the development of targeted therapeutic strategies, whereas epigenetic signatures hold promise as diagnostic, prognostic, and treatment-monitoring biomarkers. Although clinical applications remain limited, advancing knowledge of SNARE genetics and epigenetics may facilitate the development of novel diagnostic modalities, prognostic tools, and precision therapeutic strategies for neurologic diseases. - Source: PubMed
Publication date: 2026/07/06
Besin ValentinusMulyanata Lisa ThaliaHumardani Farizky Martriano - The function of the SNARE complex regulator, Munc18-1, in photoreceptor cells is unknown. Here, we found that removing Munc18-1 from photoreceptors results in major degeneration starting at P14. In the absence of Munc18-1, before major photoreceptor degeneration, functional and synaptic impairments were present, indicating a critical function of Munc18-1. Furthermore, Munc18-1 played a critical role in expression and localization of syntaxin-3. The syntaxin-3 protein level is dramatically reduced in the soma and plasma membrane of photoreceptors without Munc18-1. At the photoreceptor synapses, the colocalization of syntaxin-3 and its SNARE partner, SNAP-25, was reduced, potentially suggesting an altered syntaxin-3 synaptic localization. In the Munc18-1-deficient photoreceptors, immature synapses and outer segment lesions were found. Taken together, these findings provide evidence that Munc18-1 is important for maintaining sufficient syntaxin-3 expression in the cell body and synapses of photoreceptors. The lack of Munc18-1, combined with poor syntaxin-3 expression, contributes to photoreceptor functional impairment and degeneration. - Source: PubMed
Publication date: 2026/07/04
Huang MengjiaChow Chun HinNoworolski RyanCharish JasonIndrawinata KarenHarada HidekiyoWallace Valerie AMonnier Philippe PSugita Shuzo