更新于：2024-11-01

SV2B

更新于：2024-11-01

基本信息

别名

HsT19680、KIAA0735、SV2B

+ [1]

简介

Probably plays a role in the control of regulated secretion in neural and endocrine cells. (Microbial infection) Receptor for the C.botulinum neurotoxin type A2 (BoNT/A, botA); glycosylation is not essential but enhances the interaction (PubMed:29649119). Probably also serves as a receptor for the closely related C.botulinum neurotoxin type A1.

关联

100 项与 SV2B 相关的临床结果

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100 项与 SV2B 相关的转化医学

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0 项与 SV2B 相关的专利（医药）

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105

项与 SV2B 相关的文献（医药）

2024-04-04·Journal of Molecular Cell Biology

SV2B defines a subpopulation of synaptic vesicles

Article

作者: Wolff, Christian ; Mairet-Coello, Georges ; Musial, Timothy F ; Schoch, Susanne ; Clasadonte, Jérôme ; Beckert, Hannes ; Dietrich, Dirk ; Schmitt, Mathieu ; Gschossmann, Lena J ; Wolf, Julia ; Paulussen, Isabelle

AbstractSynaptic vesicles can undergo several modes of exocytosis, endocytosis, and trafficking within individual synapses, and their fates may be linked to different vesicular protein compositions. Here, we mapped the intrasynaptic distribution of the synaptic vesicle proteins SV2B and SV2A in glutamatergic synapses of the hippocampus using three-dimensional electron microscopy. SV2B was almost completely absent from docked vesicles and a distinct cluster of vesicles found near the active zone. In contrast, SV2A was found in all domains of the synapse and was slightly enriched near the active zone. SV2B and SV2A were found on the membrane in the peri-active zone, suggesting the recycling from both clusters of vesicles. SV2B knockout mice displayed an increased seizure induction threshold only in a model employing high-frequency stimulation. Our data show that glutamatergic synapses generate molecularly distinct populations of synaptic vesicles and are able to maintain them at steep spatial gradients. The almost complete absence of SV2B from vesicles at the active zone of wildtype mice may explain why SV2A has been found more important for vesicle release.

2024-04-01·Psychiatry Research

Neurogenetic underpinnings of nicotine use severity: Integrating the brain transcriptomes and GWAS variants via network approaches

Article

作者: Wang, Tingting ; Yang, Bao-Zhu ; Li, Chiang-Shan R ; Ma, Shuangge ; Xiang, Bo

Our study focused on human brain transcriptomes and the genetic risks of cigarettes per day (CPD) to investigate the neurogenetic mechanisms of individual variation in nicotine use severity. We constructed whole-brain and intramodular region-specific coexpression networks using BrainSpan's transcriptomes, and the genomewide association studies identified risk variants of CPD, confirmed the associations between CPD and each gene set in the region-specific subnetworks using an independent dataset, and conducted bioinformatic analyses. Eight brain-region-specific coexpression subnetworks were identified in association with CPD: amygdala, hippocampus, medial prefrontal cortex (MPFC), orbitofrontal cortex (OPFC), dorsolateral prefrontal cortex, striatum, mediodorsal nucleus of the thalamus (MDTHAL), and primary motor cortex (M1C). Each gene set in the eight subnetworks was associated with CPD. We also identified three hub proteins encoded by GRIN2A in the amygdala, PMCA2 in the hippocampus, MPFC, OPFC, striatum, and MDTHAL, and SV2B in M1C. Intriguingly, the pancreatic secretion pathway appeared in all the significant protein interaction subnetworks, suggesting pleiotropic effects between cigarette smoking and pancreatic diseases. The three hub proteins and genes are implicated in stress response, drug memory, calcium homeostasis, and inhibitory control. These findings provide novel evidence of the neurogenetic underpinnings of smoking severity.

2023-03-01·Experimental Gerontology

Cross-sectional study and bioinformatics analysis to reveal the correlations of osteoporosis in patients with Parkinson's disease

Article

作者: Li, Guanglei ; Li, Junhong ; Xiao, Erya ; Wang, Xiaoyan ; Liu, Ping ; Yu, Ronghui ; Guo, Jingjing ; Ma, Cong

OBJECTIVESOsteoporosis and Parkinson's disease (PD) are both aging-related diseases. PD patients with comorbid osteoporosis are vulnerable to the risk of fracture, which leads to a serious public health burden to the whole society. Therefore, this study sought to reveal the clinical and genetic correlations between PD and osteoporosis based on a cross-sectional study and bioinformatics analysis.METHODSA cross-sectional study of 95 PD patients and 99 healthy controls was conducted. Ordinal logistic regression analysis was utilized to investigate the clinical correlations between PD and osteoporosis. Two microarray datasets (GSE20292, GSE35958) including PD, osteoporosis and normal control samples were retrieved from the GEO database for GO analysis, KEGG pathway analysis and PPI network.RESULTSPD patients had lower 25(OH)VitD, FN BMD, BMD and T-score of the LS and TH, as well as poorer bone mass diagnosis, yet higher PINP compared to healthy controls. Both age and UPDRS II score of PD patients were adversely correlated with BMD of LS and TH. PD diagnosis acted as an independent risk factor of osteoporosis, and PD patients had approximately double risk for osteoporosis. Bioinformatics analysis further revealed that SNAP25, AQP4, SV2B, KCND3, and ABCA2 had important diagnostic value and risk prediction value for both PD and osteoporosis.CONCLUSIONSPD diagnosis can be used as an independent risk factor for osteoporosis. Moreover, SNAP25, AQP4, SV2B, KCND3 and ABCA2 as the top 5 hub genes have important diagnostic and risk predictive value for both PD and osteoporosis.