SYT1

Last update 08 May 2025

Basic Info

Synonyms

P65, SVP65, synaptotagmin 1

+ [5]

Introduction

Calcium sensor that participates in triggering neurotransmitter release at the synapse (By similarity). May have a regulatory role in the membrane interactions during trafficking of synaptic vesicles at the active zone of the synapse (By similarity). It binds acidic phospholipids with a specificity that requires the presence of both an acidic head group and a diacyl backbone. A Ca(2+)-dependent interaction between synaptotagmin and putative receptors for activated protein kinase C has also been reported. It can bind to at least three additional proteins in a Ca(2+)-independent manner; these are neurexins, syntaxin and AP2. Plays a role in dendrite formation by melanocytes (PubMed:23999003).

100 Clinical Results associated with SYT1

100 Translational Medicine associated with SYT1

0 Patents (Medical) associated with SYT1

1,180

Literatures (Medical) associated with SYT1

01 May 2025·Neural Regeneration Research

NECAB family of neuronal calcium-binding proteins in health and disease

Article

Author: Schäfer, Michael K.E. ; Methner, Axel ; Bueno, Diones ; Schmeisser, Michael J. ; Wang, Sudena

The N-terminal EF-hand calcium-binding proteins 1–3 (NECAB1–3) constitute a family of predominantly neuronal proteins characterized by the presence of at least one EF-hand calcium-binding domain and a functionally less well characterized C-terminal antibiotic biosynthesis monooxygenase domain. All three family members were initially discovered due to their interactions with other proteins. NECAB1 associates with synaptotagmin-1, a critical neuronal protein involved in membrane trafficking and synaptic vesicle exocytosis. NECAB2 interacts with predominantly striatal G-protein-coupled receptors, while NECAB3 partners with amyloid-β A4 precursor protein-binding family A members 2 and 3, key regulators of amyloid-β production. This demonstrates the capacity of the family for interactions with various classes of proteins. NECAB proteins exhibit distinct subcellular localizations: NECAB1 is found in the nucleus and cytosol, NECAB2 resides in endosomes and the plasma membrane, and NECAB3 is present in the endoplasmic reticulum and Golgi apparatus. The antibiotic biosynthesis monooxygenase domain, an evolutionarily ancient component, is akin to atypical heme oxygenases in prokaryotes but is not well-characterized in vertebrates. Prokaryotic antibiotic biosynthesis monooxygenase domains typically form dimers, suggesting that calcium-mediated conformational changes in NECAB proteins may induce antibiotic biosynthesis monooxygenase domain dimerization, potentially activating some enzymatic properties. However, the substrate for this enzymatic activity remains uncertain. Alternatively, calcium-mediated conformational changes might influence protein interactions or the subcellular localization of NECAB proteins by controlling the availability of protein–protein interaction domains situated between the EF hands and the antibiotic biosynthesis monooxygenase domain. This review summarizes what is known about genomic organization, tissue expression, intracellular localization, interaction partners, and the physiological and pathophysiological role of the NECAB family.

01 Apr 2025·Journal of Alzheimer’s Disease

Changes in transcriptional regulation in the temporal lobe in patients with Alzheimer's disease

Article

Author: Chen, Yu ; Li, Yinhu ; Yang, Yujie

BackgroundAlzheimer's disease (AD) is a complex neurodegenerative disorder with intricate pathophysiological mechanisms. Transcriptome analysis has been used to investigate the pathogenesis of AD from the perspectives of mRNA expression, alternative splicing, and alternative polyadenylation. However, these 3 transcriptomic regulatory layers have not been comprehensively explored, limiting our understanding of the transcriptomic landscapes of AD pathogenesis.ObjectiveWe aimed to describe the transcriptomic landscapes of AD pathogenesis, detect the contributions of different regulatory layers to the total transcriptional variance, and identify diagnostic candidates for AD prediction.MethodsWe collected RNA sequencing data derived from the temporal lobes of 257 patients with AD and 97 controls, performed joint transcriptional analysis with multi-omics factor analysis (MOFA2) and weighted gene co-expression network analysis (WGCNA), and evaluated the signals with regression models.Results We found that increasing Braak stage is associated with progressive downregulation of SYT1, CHN1, SNAP25, VSNL1, and ENC1 as well as upregulation of TNS1 , SGK1 , CPM , PPFIBP , and CLMN . Subsequent MOFA2 revealed that alternative splicing contributes most ( R2 = 0.558) to the transcriptional variance between patients with AD and controls followed by alternative polyadenylation ( R2 = 0.449) and mRNA expression ( R2 = 0.438). In addition, the regression model constructed with SNAP25 , VSNL1 , and ENC1 expression could distinguish between patients with AD and controls (AUC = 0.752). ConclusionsWe systematically detailed the transcriptional landscapes in patients with AD and report mRNA signals associated with AD, offering novel insights into AD pathogenesis and therapeutic development.

01 Mar 2025·Brain and Behavior

Transcriptomic Dysregulation in Animal Models of Attention‐Deficit Hyperactivity Disorder and Nicotine Dependence Suggests Shared Neural Mechanisms

Article

Author: Van Horn, Sarah ; Toufexis, Donna J ; Driscoll, Heather

ABSTRACTIntroductionAttention‐deficit‐hyperactivity disorder (ADHD) is highly heritable and increases the likelihood of nicotine dependence (ND). The self‐medication hypothesis of nicotine use in ADHD proposes that ADHD patients seek nicotine for its ability to improve their symptoms, and they have less success quitting, possibly due to the worsening of ADHD symptoms in withdrawal.MethodsThe present analysis compared transcriptomic data from the brains of rodent models of ADHD and those of ND, with a focus on striatal gene expression. Differential expression analysis, pathway enrichment analysis, and gene‐network mapping identified signaling networks and candidate genes that may contribute to the high co‐occurrence between ADHD and ND.ResultsWe identified novel differentially expressed genes (PRKAG2, MAPK1), and genes with known associations to either ADHD or ND (ANK3, CALD1, CHRNA4, CHRNA7, CMTM8, DLG4, DUSP6, GNG3, GNG11, GRIK5, GRINA2, GRM5, ICAM2, KCNJ6, PRKAB1, SNAP25, SYNPO, SYT1, VAMP2). In addition, synaptic transmission (hsa04728, R‐HAS‐112315, R‐HSA‐442755) and MAPK signaling pathways (hsa04010, hsa04014, hsa04015, R‐HSA‐5673001, R‐HSA‐5684996) were enriched in both ADHD and ND.ConclusionThe signaling pathways implicated by this analysis mediate neurological mechanisms known to contribute to ND. The association of analogous differently expressed genes and common signaling pathways suggests an important causal relationship between ND and ADHD that may be clinically important.

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SYT1

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