anti-Synapsin II (SYN2) Anticorps

Human Synapsin II (SYN2) interaction partners

1. 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.

2. Both GABRA6 and Synapsin II polymorphisms are important risk factors for the development of idiopathic generalized epilepsy in a South Indian population.

3. Results identify SYN2 as a novel predisposing gene for autism spectrum disorders (ASD) and strengthen the hypothesis that a disturbance of synaptic homeostasis underlies ASD.

4. Synapsin II is involved in the molecular pathway of lithium treatment in bipolar disorder

5. SYN2 rs3773364 A>G polymorphism is not a risk factor for susceptibility to epilepsy in this case-control study and meta-analysis.

6. 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.

7. This study suggests a positive association between synapsin II and schizophrenia, implying that synapsin II is involved in the etiology of schizophrenia.

8. synapsin II variants are associated with susceptibility to schizophrenia.

9. Syn2 is likely to be involved in the etiology or pathogenesis of schizophrenia.

10. 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.

Mouse (Murine) Synapsin II (SYN2) interaction partners

1. results reveal a permissive contribution of Syn2 to the expression of normal socio-communicative behavior

2. These results reveal a new SynII function in the regulation of the time course of GABA release and demonstrate that this function is dependent on the interneuron subtype.

3. This study demonstrated that synapsin 2 regulating GABA Release from Hippocampal Interneurons.

4. Pharmacological and knockdown experiments showed that activation of sympathetic neurons by SCFA propionate involves SCFA receptor GPR41 linking to Gbetagamma-PLCbeta3-ERK1/2-synapsin 2

5. 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.

6. This study demonostrated that Epileptic synapsin triple knockout mice exhibit progressive long-term aberrant plasticity in the entorhinal cortex.

7. In synapsin II(-) hippocampal neurons an overexcitable phenotype was observed.

8. 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.

9. Behavioral and neurophysiological features of Syn-2 knockout mice are characterized by observation of the development and progress of seizures from postnatal day 20 to 180.

10. 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.

11. Syn II promotes gamma-aminobutyric acid asynchronous release in a Ca(2+)-dependent manner.

12. Analysis of cultured neurons from wild-type and Syn I,II,III-deficient triple knock-out (TKO) mice shows that synaptic vesicles are severely dispersed in the absence of Syns.

13. We conclude that neither synapsin I nor synapsin II are directly involved in the regulation of glucose-stimulated insulin secretion and Ca(2)-dependent exocytosis in mouse pancreatic beta-cells.

14. Synapsin I and II affect distinct excitatory glutamatergic synapses in the hippocampus, synapsin-dependent modulations of synaptic function may use distinct presynaptic response patterns to induce different classes of presynaptic plasticity.[Review]

15. The supply rate of vesicle trafficking depresses more rapidly in synapsin knock-outs; the phenotype can be fully explained by changing the value of the single parameter in the model that would specify the size of the local reserve pools.

16. findings suggest that seizure behavior in synapsin I and synapsin II KO mice is not solely determined by cortical activity but rather reflects interplay between cortical activity and activity in other brain regions

17. Taken together, our results suggest that synapsin II and Rab3a have separate roles in maintaining the total store of synaptic vesicles and cooperate in promoting the latest steps of neuronal secretion.

18. study provided high sequence coverage information on synapsin 2a and 2b in mouse and rat, revealing highest identity between the species; phosphorylation sites were determined

19. Results indicate that a cAMP/PKA-dependent mechanism involving the AP-2alpha transcription factor is likely responsible for the increase in neuronal synapsin II following dopamine D1 receptor stimulation or dopamine D2 receptor inhibition.

20. synapsin II can regulate vesicle clustering, transmitter release, and facilitation.