SNAP_25 pAb
- Known as:
- SNAP_25 pAb
- Catalog number:
- ASAVAP-SV002E
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- SNAP_25 pAb
Related genes to: SNAP_25 pAb
- 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 pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(S)_Nitroso_N_acetylpenicillamine SNAP0.2ml PCR 8-strip Tubes with Snap Flat cap, color: Clear10ML CENT W SNAP12x32mm, Standard Opening Snap Vials 2mL, Amber Glass, Flat Base, 11mm Snap Vial, Standard Opening, With label.12x32mm, Standard Opening Snap Vials 2mL, Amber Glass, Flat Base, 11mm Snap Vial, Standard Opening.12x32mm, Standard Opening Snap Vials 2mL, Clear Glass, Flat Base, 11mm Snap Vial, Standard Opening, With label.12x32mm, Standard Opening Snap Vials 2mL, Clear Glass, Flat Base, 11mm Snap Vial, Standard Opening.14-3-3 β (Q69) pAb host: Rabbit14-3-3 β pAb host: Rabbit14-3-3 γ (M81) pAb host: Rabbit14-3-3 ε (D238) pAb host: Rabbit14-3-3 ε pAb host: Rabbit14-3-3 ζ (A79) pAb host: Rabbit Related articles to: SNAP_25 pAb
- Nuclear receptor corepressor 1 (NCoR1) and silencing mediator of retinoic acid and thyroid hormone (SMRT) are critical regulators that mediate transcriptional repression through histone deacetylation. Despite high structural homology, their distinct roles in the central nervous system remain poorly understood. To elucidate these roles, we generated neuronal-specific NCoR1 or SMRT knockout mice using Snap25-IRES2-Cre mice. Behavioral assessments revealed that while both NCoR1 and SMRT deficiency led to hypoactivity, social deficits, and mild anxiety, NCoR1-deficient mice uniquely exhibited enhanced learning abilities in a visual discrimination task, indicating functional separation in cognitive regulation. This divergence was supported by RNA-sequencing in the amygdala at postnatal day 21 (PND 21), where SMRT deletion upregulated 449 genes, whereas NCoR1 deletion upregulated only 8 genes. Furthermore, we investigated the protein stability of HDAC3, the primary enzymatic partner of these corepressors. At PND 21, HDAC3 levels were significantly reduced in the NCoR1-deficient hippocampus but significantly increased in the SMRT-deficient amygdala. In contrast, HDAC3 levels remained stable in the adult cerebellum and PND 3 cerebrum regardless of corepressor status. Notably, while mice with deletion of both NCoR1 and SMRT exhibit early postnatal lethality, their HDAC3 levels were unchanged compared to controls at PND 3, suggesting that the lethal phenotype is not primarily driven by a systemic loss of HDAC3 protein. Collectively, our findings demonstrate that NCoR1 and SMRT function through independent transcriptional networks and context-dependent regulatory mechanisms. This study highlights the specialized, non-redundant roles of these homologous corepressors in the brain according to developmental stage and region. - Source: PubMed
Publication date: 2026/06/10
Amano IzukiRitter Megan JNinomiya AyaneKawabata-Iwakawa ReikaVierling TaylorCespedes Isabella SalgueroHollenberg Anthony NKoibuchi Noriyuki - Although changes in the lung microbiome have been observed in many respiratory diseases, the lung microbiome of patients with tuberculosis (TB) remains largely undefined. The aim of this study was to determine and compare the composition of upper and lower respiratory microbial communities, changes in host gene expression, and functional pathway activation in patients with TB and community-acquired pneumonia using a Metatranscriptomic approach. - Source: PubMed
Publication date: 2026/06/06
Li LiangyuXu MengLiu MenglingMao JieyuXiong PeiLi RuiyunChen JianjunWu Xiaojun - Temporal lobe epilepsy (TLE) exhibits marked lateralized gray matter alterations, yet whole-brain network vulnerability patterns, particularly those independent of seizure laterality, remain incompletely understood. Furthermore, the spatial correspondence between macroscopic network disruptions and underlying molecular architectures lacks systematic characterization, limiting mechanistic insights into epileptic network pathology. We utilized voxel-based morphometry (VBM) and surface-based morphometry (SBM) to characterize whole-brain gray matter alterations in 69 TLE patients (34 left-TLE, 35 right-TLE for lateralization analysis) and 47 controls. Twelve multivariate machine learning algorithms were employed to validate the robustness and importance of structural features. Additionally, imaging-transcriptomics analyses using the Allen Human Brain Atlas were conducted to examine spatial associations between gene expression profiles and brain morphological alterations. Beyond lateralization-specific atrophy, we identified bilateral somatomotor and default mode networks, along with the right ventral attention network, as primary vulnerable networks independent of seizure origin (all P < 0.05). Machine learning confirmed right somatomotor network atrophy as a structurally robust signature of TLE. Imaging-transcriptomics analysis revealed a striking correspondence between cortical network atrophy and synaptic genes related to signaling and structural organization. Specifically, we uncovered distinct spatial covariation profiles among four synaptic hub genes: while CTNNB1, NLGN1, and GRM5 exhibited positive spatial correlations with atrophy patterns, SNAP25 displayed an inverse relationship. This study delineates lateralization-independent vulnerability networks in TLE and characterizes their spatial-molecular architecture. By linking macroscopic atrophy to microscopic synaptic signatures, our findings present a structural-molecular framework that offers insights for future mechanistic studies and highlights potential targets for synapse-based precision therapeutic strategies. - Source: PubMed
Publication date: 2026/06/02
Zhou QinQin LuSu ShujunWeng GuimingFan BinglinChen ZexiangPang XiaominLuo CuimiQin BailingChen XuemeiYu LuQu ChuanyongHu HuoyouSun YutingZheng Jinou - Botulism is a severe neuroparalytic syndrome caused by botulinum neurotoxins (BoNTs)-among the most potent biological agents-with an estimated human lethal dose (LD) of approximately 1 ng/kg. By cleaving soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins at cholinergic nerve terminals, BoNTs block acetylcholine release, producing potentially fatal flaccid paralysis. Despite advances in supportive care, current therapeutic options remain limited to antitoxin administration, which is effective only against circulating toxin and cannot neutralize intracellular BoNT. Consequently, patients often require prolonged mechanical ventilation and rehabilitation. To address these limitations, this review provides a comprehensive overview of botulism, spanning historical recognition, structural and mechanistic insights into BoNT activity, clinical manifestations, and current treatment strategies, while highlighting therapeutic gaps. Particular emphasis is placed on emerging preclinical interventions, including small-molecule inhibitors, antibody-based therapeutics, intracellular clearance strategies, and gene- and RNA-based modalities, reflecting rapid progress in structural biology and pharmacology. Collectively, these advances highlight both the promise and the remaining translational challenges of developing next-generation countermeasures, with implications for clinical management and biodefense preparedness. - Source: PubMed
Publication date: 2026/06/02
Almudimeegh Sultan - Diabetes mellitus is a chronic disease caused by insulin uptake or deficiency. Side effects of diabetes are numerous, according to the severity of the disease. Diabetes could harm the peripheral nerves, with chronic pain leading to nerve damage known as diabetic neuropathy (DN). Signs and symptoms of DN are sharp pains, numbness, and tingling. Distal symmetric polyneuropathy is the most common nerve injury during DN. Accordingly, this study screens candidate genes related to sural nerve DN (SDN) to find the critical ones. - Source: PubMed
Publication date: 2025/07/01
Mansouri VahidRezaei-Tavirani MostafaOkhovatian Farshad