VAMP2 (Synaptobrevin) Rabbit pAb
- Known as:
- VAMP2 (Synaptobrevin) Rabbit pAb
- Catalog number:
- ASAVAS-SV006D
- Product Quantity:
- 50 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- VAMP2 (Synaptobrevin) Rabbit pAb
Related genes to: VAMP2 (Synaptobrevin) Rabbit pAb
- Gene:
- VAMP2 NIH gene
- Name:
- vesicle associated membrane protein 2
- Previous symbol:
- SYB2
- Synonyms:
- VAMP-2
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-14
- Date modifiied:
- 2015-11-05
Related products to: VAMP2 (Synaptobrevin) Rabbit pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host RabbitExtraction-freeCE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host: Rabbit, Extraction-free, CE-marked Related articles to: VAMP2 (Synaptobrevin) Rabbit pAb
- Parkinson's disease (PD) and related Parkinsonian conditions involve progressive disruption of mitochondrial homeostasis, redox balance, synaptic function, and proteostasis. Available therapies remain predominantly symptomatic, motivating the search for multitarget compounds acting across stress-sensitive pathways. BjPro-7a (pEDGPIPP), a proline-rich oligopeptide from Bothrops jararaca venom, exerts cytoprotective effects under oxidative stress, but its activity in an in vivo Parkinsonian-like model is unknown. Here we investigated whether BjPro-7a attenuates the behavioral and proteomic disturbances induced by 1-methyl-4-phenylpyridinium (MPP) in zebrafish larvae. Larvae were exposed to 500 µM MPP and post-treated with 10 µM BjPro-7a, followed by assessment of basal locomotion, light/dark-evoked behavior, and label-free proteomic profiling. BjPro-7a markedly reversed the MPP-induced hypolocomotor phenotype by increasing the total distance traveled, improving bout-related parameters, reducing inter-episode intervals, and restoring visually evoked responsiveness. Proteomic analysis revealed broad rescue-associated remodeling, more pronounced among proteins suppressed by MPP than among those elevated by intoxication. Functional enrichment and protein-protein interaction analyses indicated coordinated modulation of vesicle trafficking and synaptic organization, mitochondrial and bioenergetic function, redox homeostasis, and protein quality control. Representative rescue-associated proteins included VAMP2 and SNAP25A (synaptic), SDHA and UQCRFS1 (mitochondrial), G6PD and PRDX3 (redox), and PSMC5 and STIP1 (proteostasis). Together, these findings show that BjPro-7a attenuates MPP-induced dysfunction and promotes systems-level proteomic remodeling consistent with rescue in zebrafish larvae. These data support BjPro-7a as a promising candidate for future therapeutic studies in Parkinsonian-like neurotoxicity. - Source: PubMed
Publication date: 2026/07/13
Maleski Adolfo Luis Almeidada Cunha E Silva Felipe AssumpçãoPereira Bruno FioreliniAlberto-Silva Carlos - Terahertz (THz) waves, with frequencies between those of microwaves and infrared light, can excite nonlinear resonance and affect cellular function. However, the effects and underlying mechanism of terahertz radiation on neurons and rodent behaviour are still unclear. Here, we constructed THz radiation exposure models in the perirhinal cortex (PRH) of male mice. First, we measured the power and depth of penetration of the 0.152 THz photons cranially above the PRH. We demonstrated that the visual recognition memory of mice was improved after THz wave irradiation, which was similar to the effect of light activation of glutamatergic neurons in the PRH. In addition, THz wave exposure increased the number of c-Fos neurons, synchronous electrical activity, synaptic plasticity and glutamatergic neuronal excitability in the PRH. Moreover, the expression of molecules involved in glutamate transmission, such as VAMP2, EAAT, CaMKII and PSD95, increased along with enhanced NMDAR and AMPAR activity. Our findings revealed that THz waves could improve recognition memory via the activation of excitatory neurons and accelerated glutamate metabolism in the PRH, suggesting that THz photon stimulation might be developed as a noninvasive neuromodulation technique to promote cognitive function. - Source: PubMed
Publication date: 2026/07/06
Wang HuiHe ZhiweiSong LequanDong JiPan JunmiaoCheng WenjingWang RuiWang YuqingZhao LiPeng Ruiyun - 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 - Synaptic transmission occurs synchronously with real-world events, far faster than vesicle fusion for hormone release or membrane biogenesis, all mediated by soluble -ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complexes. How SNAREs cooperate to achieve synchronous neurotransmitter release is a long-standing mystery. Rapid release (<7 milliseconds) has been reconstituted from purified synaptic SNAREs, SNARE-assembling chaperones, and calcium ion sensors in a fully-defined, genetically validated system that enables single-molecule counting in docked vesicles before release. SNAREpin complexes (12 ± 0.3) are found in each such ready-release vesicle, suggesting a regular structure. Several genetic conditions (including point mutation of the synaptic vesicle protein Synaptophysin from a Synaptopathy patient and human and mouse disease mutations of the synaptic vesicle protein vesicle-associated membrane protein-2 (VAMP2) reduce the number of SNAREpins to 6 ± 0.3 and result in profoundly delayed release over 0.1 to 1 seconds. Omitting Synaptophysin, whose hexamers preassemble 12 copies of VAMP2, also yields ~6 SNAREpins and delays release. - Source: PubMed
Publication date: 2026/07/01
Bera ManindraChatterjee AtrouliAji Amit KoikkarahPanda AniruddhaSundaram R Venkat KColeman JeffMaroofian RezaSalpietro VincenzoRadhakrishnan AbhijithGautam SudhanshuGrushin KirillCaruel MatthieuHoulden HenryGupta KallolRamakrishnan SathishPincet FredericRothman James E