anti-Synapsin I (SYN1) Antibodies

Human Synapsin I (SYN1) interaction partners

1. A surface-based group study using novel diffusion and quantitative multiparametric imaging on 13 SYN1Q555X mutation carriers and 13 age- and sex-matched controls. Results showed significant microstructural alterations in several regions usually involved in oral and written language as well as dyslexia. The most significant changes in these regions were lowered mean diffusivity and increased fractional anisotropy.

2. Authors identified the c.236 C > G/p.S79W mutation in SYN1 as causative for the non-syndromic ID of the MRX50 family. Accordingly, the in vitro characterization of S79W SynI clearly indicates that the mutation does not interfere with neurodevelopmental aspects, but perturbs spontaneous SV exocytosis, SV clustering and SV lateral mobility along axons.

3. 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.

4. Cerebral malaria causes pre-synaptic excitation and eventually activation of synapsin I, leading to increased neurotransmitter release.

5. Patterns of the immunoreactivity with antibodies to SNAP-25, synapsin-I and synaptophysin are completely appropriate to those of adult's OB on the 38-40 weeks of the prenatal development.

6. The implementation of the AlphaScreen pSYN1 assay and future development of additional primary neuronal HTS assays provides an attractive approach for discovery of novel classes of therapeutic candidates for a variety of CNS disorders.

7. these findings suggest PRICKLE1 mutations contribute to ASD by disrupting the interaction with SYN1 and regulation of synaptic vesicles.

8. Data indicate that in patients carrying the W356x mutation the function of synapsin I is markedly impaired, and support the value of Syn1(-/-) mice as an experimental model mimicking the human pathology.

9. Epileptogenic Q555X SYN1 mutant triggers imbalances in release dynamics and short-term plasticity.

10. The histone modification marks were significantly increased in major depression and this effect was correlated with significant increases in SYN1b gene expression.

11. A conserved region of human and mouse SYN1 promoters contains cis-sites for the transcriptional activator Sp1 in close proximity to REST binding motifs.

12. The allelic frequencies of SYN1 are associated with Korean female schizophrenia.

13. SYN1 loss-of-function mutations in autism and partial epilepsy cause impaired synaptic function.

14. the nucleocytoplasmic shuttling of dysbindin-1 regulates synapsin I expression and thus may be involved in the pathogenesis of schizophrenia.

15. The authors propose claudin-2 and SYN1 work in concert to enhance microbial translocation across the intestinal epithelial barrier to contribute to chronic immune activation and CD4 T-cell depletion in HIV-1-infected patients.

16. The results showed that synapsin I was significantly decreased in the stratum radiatum of CA1 subfield and the molecular layer of DG in AD patients.

17. SYN1 nonsense mutation is the likely cause of epileptic and other phenotypes

18. Synapsins and S100A1 interact in nerve terminals where coexpresssed; S100A1 cannot bind SV-associated synapsin I and may function as a cytoplasmic store of monomeric synapsin I; synapsin dimerization and interaction with S100A1 are mutually exclusive

19. This study concluded that the human synapsin I gene is positively regulated by nuclear respiratory factor 1 and mediates the function of nuclear respiratory factor 1 in neurite outgrowth.

Mouse (Murine) Synapsin I (SYN1) interaction partners

1. Results implicate SYN1 in the pathogenesis of non-syndromic intellectual disability, showing that alterations of synaptic vesicle trafficking are one possible cause of this disease, and suggest that distinct mutations in SYN1 may lead to distinct brain pathologies.

2. This study demonstrated that syn1 affect the rate of release of GABA quanta residing within the Hippocampal Interneurons.

3. Synapsin I is localized and produced at mature axon terminals and at immature growth cones.

4. HSV-1-infected neurons also exhibite significantly reduced expression of the presynaptic proteins synapsin-1 and synaptophysin. These effects depended on GSK-3 activation and intraneuronal accumulation of Ab

5. Functions of synapsins in corticothalamic facilitation: important roles of synapsin I

6. Levels of synapsin Ia/b increased in contralateral visual cortex following monocular deprivation.

7. SynI mRNA and protein levels are down-regulated in the hippocampus of naive and Morris water maze-treated En2-/- mice.

8. age-dependent reduction of phospho-synapsin-Ia reversed by exercise regimen

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

10. these findings suggest PRICKLE1 mutations contribute to ASD by disrupting the interaction with SYN1 and regulation of synaptic vesicles.

11. during chronic modification of neuronal activity and is an essential downstream effector for the Cdk5-mediated homeostatic scaling.

12. O-GlcNAcylation of Thr-87 interferes with folding of the ALPS motif, providing a means for regulating the association of synapsin I with SVs as a mechanism contributing to synapsin I localization and RPSV generation.

13. Data indicate that in patients carrying the W356x mutation the function of synapsin I is markedly impaired, and support the value of Syn1(-/-) mice as an experimental model mimicking the human pathology.

14. Epileptogenic Q555X SYN1 mutant triggers imbalances in release dynamics and short-term plasticity.

15. 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.

16. the serine residue at 605 of the synapsin-1 peptide, 603QASQAGPGPR612, and the serine residue at 692 of the tau peptide, 688SPVVSGDTSPR698, were found to be potential reciprocal O-GlcNAcylation and phosphorylation sites.

17. Synapsin I knock-out mice do not exhibit a linear progression of the epileptic seizure phenotype.

18. post-receptor calcium-dependent mechanisms associated with nicotine withdrawal are mediated through beta2-containing nicotinic receptors.

19. NPAS4 plays an important role in the structural and functional plasticity of neurons

20. A conserved region of human and mouse SYN1 promoters contains cis-sites for the transcriptional activator Sp1 in close proximity to REST binding motifs.

Cow (Bovine) Synapsin I (SYN1) interaction partners

1. These results raise the possibility that Ser(603) on synapsin I is alternatively phosphorylated by p21-activated kinases, not only by CaMKII, in neuronal cells in response to some stimulants.

2. Synapsin acts as a phosphorylation-modulated mediator of feedback regulation of Gz signaling by the synaptic machinery

3. Synapsin-Rab3 interaction may participate in the regulation of synaptic vesicle trafficking within the nerve terminals.

4. Interacts with rab3 protein; this interaction is likely to play a major role in the modulation of neurotransmitter release.

Pig (Porcine) Synapsin I (SYN1) interaction partners

1. This study reports molecular cloning and characterization of the coding sequence of the porcine ortholog of syn I, including identification and verification at the protein level of an alanine-encoding insert.