Ask about this productRelated genes to: Vamp1 Blocking Peptide
- Gene:
- VAMP1 NIH gene
- Name:
- vesicle associated membrane protein 1
- Previous symbol:
- SYB1
- Synonyms:
- VAMP-1
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-14
- Date modifiied:
- 2016-10-05
Related products to: Vamp1 Blocking Peptide
Related articles to: Vamp1 Blocking Peptide
- The mechanisms through which chronic stress-related genes influence the diagnosis of osteoporosis (OP), where chronic stress serves as a risk factor, remain unclear. This study aimed to identify chronic stress-related biomarkers using multi-omics approaches and explore their potential applications in the diagnosis and treatment of OP. - Source: PubMed
Publication date: 2026/06/09
Fang HuangHe Rui - Lethal-wasting (lew) is a spontaneous null mutation in the gene encoding the vesicular SNARE protein synaptobrevin 1 (SYB1/VAMP1). Homozygous mice exhibit profound impairment in neuromuscular transmission and die around three weeks after birth. Pathogenic variants in human SYB1 are associated with a variety of disorders such as hereditary spastic ataxia and congenital myasthenic syndrome. Although Syb1 expression is highly enriched in neurons, it has also been reported in non-neuronal tissues, raising the possibility that non-neuronal defects contribute to the lethal phenotype. Here, we tested whether neuronal dysfunction is the primary cause of death in mice and whether the closely related isoform synaptobrevin 2 (Syb2/VAMP2) can substitute for Syb1functin . We show that neuron-specific expression of in mice fully rescues lethality in mice, restoring normal growth and motor function. Electrophysiological analyses demonstrate complete recovery of neuromuscular synaptic transmission, including spontaneous and evoked release as well as short-term plasticity. These findings establish that neuronal expression of ECFP-Syb2 is sufficient to prevent the lethal phenotype associated with Syb1 deficiency and demonstrate that Syb2 can functionally replace Syb1 at motor nerve terminals . - Source: PubMed
Publication date: 2026/05/26
Liu YunYe QiaohongLin Weichun - The etiology of idiopathic sudden sensorineural hearing loss (iSSNHL) remains unclear, and genome-wide genetic evidence is limited. We conducted a multicenter Japanese case-control genome-wide association study including 192 clinically defined iSSNHL cases and 15,302 controls aged ≥80 years without a history of hearing loss. After cross-platform SNP harmonization and imputation (Eagle/Minimac4), association testing was performed using dosage-based logistic regression in PLINK 2.0, adjusting for sex and principal components (PC1-PC10). Gene- and pathway-level analyses were conducted using MAGMA and the PANTHER overrepresentation test. Genomic inflation was modest (λ_GC = 1.04). Eight loci reached genome-wide significance ( < 5 × 10), led by , with additional loci near , , , , , , and ; 21 loci met the suggestive threshold ( < 1 × 10). MAGMA identified eight genes at FDR < 0.05 (, , , , , , , and ). These findings suggest that immune-inflammatory and cellular stress-homeostasis mechanisms may contribute to iSSNHL susceptibility and provide candidate loci for future replication and functional studies. - Source: PubMed
Publication date: 2026/02/14
Kitoh RyosukeNishio Shin-YaTakumi YutakaUsami Shin-Ichi - Alzheimer's disease (AD) is characterized by widespread molecular dysregulation, with the APOEe4 allele recognized as its strongest genetic risk factor. However, the mechanisms by which APOEe4 drives distinct molecular changes - whether by exacerbating pathology or triggering compensatory responses - remain incompletely understood. We generated and analyzed proteomic, epigenetic, and genetic data from post-mortem dorsolateral prefrontal cortex samples of a uniquely APOEe4-enriched subset of the Religious Orders Study and Memory and Aging Project (ROSMAP). Specifically, we generated DIA LC-MS proteomic data (n = 302), analyzed previously generated DNA methylation profiles from our group (n = 310), and used published whole-genome sequencing data (n = 254) to compute polygenic risk scores (PRS). In this cohort, 69% (n = 214) were APOEe4 carriers, and 19.6% (n = 42) of them showed no pathological evidence of AD based on NIA-Reagan criteria, enabling identification of APOEe4-related risk and resilience mechanisms. In the absence of AD, APOEe4 carriers exhibited lower levels of 27 proteins, suggesting early synaptic (e.g., VAMP1, SYN3, CASKIN1) and metabolic (e.g., GLUD1, PI4KA) vulnerability. By contrast, APOEe4 carriers with AD displayed marked upregulation of inflammatory and proteostatic proteins (e.g., GNAO1, AHNAK, FGG, HEBP1, APEX1, RAB4A, SLC12A5, LRP1, BAG6) and hypermethylation of cg06329447 in ELAVL4. Network analyses highlighted convergent disruptions in synaptic transmission, metabolism, and proteostasis - key pathways altered in APOEe4-associated AD. Mediation analyses identified GRIPAP1 and GSTK1 as top protein mediators (accounting for ~26-33% of APOEe4's effect), with VAMP1, CASKIN1, DPP3, SYN3, and FGG each contributing ~9-15%. ELAVL4 hypermethylation also mediated ~12% of the APOEe4 effect, linking epigenetic dysregulation to disease risk. To assess whether the identified proteins reflected broader genetic risk for AD or were specific to APOEe4, we calculated PRS both excluding and including the APOE genomic region. While the non-APOE PRS showed no association with identified molecular markers, the APOE-inclusive PRS was significantly associated with eight AD-related proteins in carriers, indicating they are not explained by polygenic risk outside of APOE. Finally, predictive modeling stratified by APOEe4 status revealed that in non-carriers, PRS most effectively classified AD (AUC = 0.73), whereas in carriers, proteomic and epigenetic markers outperformed PRS (AUC up to 0.74). Together, these findings demonstrate that APOEe4 confers AD risk through early synaptic and metabolic disruptions and later-stage inflammatory and epigenetic changes, laying the groundwork for genotype-tailored biomarker development and therapeutic strategies. - Source: PubMed
Publication date: 2025/10/16
Markov YaroslavPriyanka AhanaXu LeqiWang WeiweiThrush-Evensen KyraGonzalez JohnBorrus DanielKasamoto JessicaSehgal RaghavZou GraceFraij JenelCarlyle Becky CHorvath SteveBennett David AZhao Hongyuvan Dyck Christopher HLam TuKiet TLevine Morgan EHiggins-Chen Albert T - To explore the potential the role of miR-151a-5p in sperm dysfunction and its association with DNA fragmentation, mitochondrial dysfunction, and male infertility. - Source: PubMed
Publication date: 2025/11/11
Lin XiaotingGuo JiamingWang XiboXiao XiSun JieDing WenPeng YunYan Hongli