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SYN1 is a member of the synapsin gene family.
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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.
These findings contribute to previous work showing dysregulation of Synapsins, particularly SYN2 (Montrer SYN2 Kits ELISA), in mood disorders and improve our understanding of the regulatory mechanisms that precipitate these changes likely leading to the BD or MDD phenotype.
Cerebral malaria causes pre-synaptic excitation and eventually activation of synapsin I, leading to increased neurotransmitter release.
Patterns of the immunoreactivity with antibodies to SNAP-25 (Montrer SNAP25 Kits ELISA), synapsin-I and synaptophysin (Montrer SYP Kits ELISA) are completely appropriate to those of adult's OB on the 38-40 weeks of the prenatal development.
The implementation of the AlphaScreen pSYN1 assay and future development of additional primary neuronal HTS (Montrer APCDD1 Kits ELISA) assays provides an attractive approach for discovery of novel classes of therapeutic candidates for a variety of CNS disorders.
these findings suggest PRICKLE1 mutations contribute to ASD (Montrer ARSD Kits ELISA) by disrupting the interaction with SYN1 and regulation of synaptic vesicles.
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.
Epileptogenic Q555X SYN1 mutant triggers imbalances in release dynamics and short-term plasticity.
The histone modification marks were significantly increased in major depression and this effect was correlated with significant increases in SYN1b gene expression.
A conserved region of human and mouse SYN1 promoters contains cis-sites for the transcriptional activator Sp1 (Montrer PSG1 Kits ELISA) in close proximity to REST binding motifs.
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.
This study demonstrated that syn1 affect the rate of release of GABA quanta residing within the Hippocampal Interneurons.
Synapsin I is localized and produced at mature axon terminals and at immature growth cones.
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
Functions of synapsins in corticothalamic facilitation: important roles of synapsin I
SynI mRNA and protein levels are down-regulated in the hippocampus of naive and Morris water maze-treated En2 (Montrer EN2 Kits ELISA)-/- mice.
these findings suggest PRICKLE1 mutations contribute to ASD (Montrer GUSB Kits ELISA) by disrupting the interaction with SYN1 and regulation of synaptic vesicles.
during chronic modification of neuronal activity and is an essential downstream effector for the Cdk5 (Montrer CDK5 Kits ELISA)-mediated homeostatic scaling.
O-GlcNAcylation of Thr (Montrer TRH Kits ELISA)-87 interferes with folding of the ALPS motif, providing a means for regulating the association of synapsin I with SVs (Montrer FGFR2 Kits ELISA) as a mechanism contributing to synapsin I localization and RPSV generation.
These results raise the possibility that Ser (Montrer SIGLEC1 Kits ELISA)(603) on synapsin I is alternatively phosphorylated by p21 (Montrer CDKN1A Kits ELISA)-activated kinases, not only by CaMKII (Montrer CAMK2G Kits ELISA), in neuronal cells in response to some stimulants.
Synapsin-Rab3 interaction may participate in the regulation of synaptic vesicle trafficking within the nerve terminals.
Interacts with rab3 protein; this interaction is likely to play a major role in the modulation of neurotransmitter release.
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.
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 plays a role in regulation of axonogenesis and synaptogenesis. The protein encoded serves as a substrate for several different protein kinases and phosphorylation may function in the regulation of this protein in the nerve terminal. Mutations in this gene may be associated with X-linked disorders with primary neuronal degeneration such as Rett syndrome. Alternatively spliced transcript variants encoding different isoforms have been identified.
brain protein 4.1
, synapsin 1
, synapsin I