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SYN2 is a member of the synapsin gene family. Zusätzlich bieten wir Ihnen Synapsin II Antikörper (34) und Synapsin II Kits (1) und viele weitere Produktgruppen zu diesem Protein an.
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These findings contribute to previous work showing dysregulation of Synapsins, particularly SYN2, in mood disorders and improve our understanding of the regulatory mechanisms that precipitate these changes likely leading to the BD or MDD phenotype.
Both GABRA6 (zeige GABRA6 Proteine) and Synapsin II polymorphisms are important risk factors for the development of idiopathic generalized epilepsy in a South Indian population.
Results identify SYN2 as a novel predisposing gene for autism spectrum disorders (ASD (zeige ARSD Proteine)) and strengthen the hypothesis that a disturbance of synaptic homeostasis underlies ASD (zeige ARSD Proteine).
Synapsin II is involved in the molecular pathway of lithium treatment in bipolar disorder
SYN2 rs3773364 A>G polymorphism is not a risk factor for susceptibility to epilepsy in this case-control study and meta-analysis.
Results from our study indicate the involvement of SYN2 gene polymorphism in conferring risk to epilepsy; however, the genetic variant does not seem to modulate drug-response in epilepsy pharmacotherapy.
This study suggests a positive association between synapsin II and schizophrenia, implying that synapsin II is involved in the etiology of schizophrenia.
synapsin II variants are associated with susceptibility to schizophrenia.
Syn2 is likely to be involved in the etiology or pathogenesis of schizophrenia.
A case-control study with synapsin II was conducted in 506 bipolar disorder patients and 507 healthy individuals from the Han Chinese population. No association was found in this study.
This study demonstrated that synapsin 2 regulating GABA Release from Hippocampal Interneurons.
Pharmacological and knockdown experiments showed that activation of sympathetic neurons by SCFA propionate involves SCFA receptor GPR41 (zeige FFAR3 Proteine) linking to Gbetagamma-PLCbeta3-ERK1/2-synapsin 2
Deletion of synapsin II, a presynaptic protein contributing to epilepsy predisposition in humans, leads to a loss of tonic inhibition in mouse hippocampal slices due to a dramatic decrease in presynaptic asynchronous GABA release.
In synapsin II(-) hippocampal neurons an overexcitable phenotype was observed.
This study demonstrated a seizure-inducing potential of regular handling in both Syn1KO and Syn2KO mice during a period between P21 and 4 1/2 months of age.
Behavioral and neurophysiological features of Syn-2 (zeige STX2 Proteine) knockout mice are characterized by observation of the development and progress of seizures from postnatal day 20 to 180.
The histone modification marks were significantly increased in bipolar disorder and major depression and this effect was correlated with significant increases in syn2 gene expression.
Syn (zeige SYP Proteine) II promotes gamma-aminobutyric acid asynchronous release in a Ca(2 (zeige CA2 Proteine)+)-dependent manner.
Analysis of cultured neurons from wild-type and Syn (zeige SYP Proteine) I,II,III-deficient triple knock-out (TKO (zeige MRPS12 Proteine)) mice shows that synaptic vesicles are severely dispersed in the absence of Syns.
We conclude that neither synapsin I (zeige SYN1 Proteine) nor synapsin II are directly involved in the regulation of glucose-stimulated insulin (zeige INS Proteine) secretion and Ca(2 (zeige CA2 Proteine))-dependent exocytosis in mouse pancreatic beta-cells.
This gene is a member of the synapsin gene family. Synapsins encode neuronal phosphoproteins which associate with the cytoplasmic surface of synaptic vesicles. Family members are characterized by common protein domains, and they are implicated in synaptogenesis and the modulation of neurotransmitter release, suggesting a potential role in several neuropsychiatric diseases. This member of the synapsin family encodes a neuron-specific phosphoprotein that selectively binds to small synaptic vesicles in the presynaptic nerve terminal. The TIMP4 gene is located within an intron of this gene and is transcribed in the opposite direction. Mutations in this gene may be associated with abnormal presynaptic function and schizophrenia. Alternative splicing of this gene results in two transcripts.
, synapsin IIa
, synapsin 2