Disease relevance of SYN2

• A hybrid gene consisting of the Escherichia coli chloramphenicol acetyltransferase gene under the control of 837 base pairs of the synapsin II 5'-upstream region was transfected into neuronal and nonneuronal cells [1].
• To investigate the possible interaction of synapsin II with actin filaments, we expressed synapsin II in Spodoptera frugiperda and High Five insect cells using a recombinant baculovirus [2].

Psychiatry related information on SYN2

• Using a cDNA microarray representing 6794 distinct human genes, we identified candidate genes whose expression is altered in cerebral cortex of cases of early Alzheimer's disease (AD); among these was the synaptic vesicle protein synapsin II, which plays an important role in neurotransmitter release [3].

High impact information on SYN2

• Two of the most consistently changed transcripts in the PSYN functional gene group, N-ethylmaleimide sensitive factor and synapsin II, were decreased in ten of ten and nine of ten subjects with schizophrenia, respectively [4].
• Synapsin II has been proposed as a candidate gene for vulnerability to schizophrenia on the basis of its function and its location in a region of the genome implicated by linkage studies in families with schizophrenia [5].
• Synapsin I, synapsin II, and synaptophysin: marker proteins of synaptic vesicles [6].
• The high degree of homology between the synapsins suggests that some of the functional properties of synapsin I are also shared by synapsin II [7].
• Synapsin II is a neuron-specific phosphoprotein that selectively binds to small synaptic vesicles in the presynaptic nerve terminal [1].

Biological context of SYN2

• However, there was no correlation between reporter gene expression in the transfected cells and endogenous synapsin II immunoreactivity [1].
• We postulate that zif268/egr-1 and PEA3 couple extracellular signals to long-term responses by regulating synapsin II gene expression [1].
• The synapsin II gene is located on 3p25, a region that has been implicated to be associated with schizophrenia by genetic linkage [8].
• The three-way haplotype analyses also revealed a significant association of SYN2 with schizophrenia (P < 0.001 after Bonferroni correction) [9].
• METHODS: Six single nucleotide polymorphisms (SNPs) and one 5-bp insertion/deletion in SYN2 and five SNPs in CPLX2 were genotyped in 154 Korean patients with schizophrenia and 133 control patients using direct sequencing or restriction fragment length polymorphism analysis [9].

Anatomical context of SYN2

• In myogenic satellite cells, initiating differentiation resulted in a decrease in SYN 2 expression and an increase in GPC 1 expression [10].
• The expression of synapsin II and N-ethylmaleimide-sensitive fusion protein (NSF) mRNAs is reported to decrease in the prefrontal cortex of these patients [11].

Associations of SYN2 with chemical compounds

• All treatments modified levels of actin isoforms, whereas both fluoxetine and GR205171 reduced synapsin II [12].

Other interactions of SYN2

• We therefore speculate that the human TIMP4 gene will be located in intron V of the human synapsin-II gene on chromosome 3p25, and we present preliminary evidence that a human synapsin-IV gene is located near the TIMP2 gene on chromosome 17q23-q25 [13].
• The SYN 2 and SYN 4 expression exhibited a similar pattern during embryonic p. major muscle development, which remained constant from ED 14 to ED 22 and declined sharply from ED 22 to ED 24 to a very low level [10].
• A quantitative study on the expression of synapsin II and N-ethylmaleimide-sensitive fusion protein in schizophrenic patients [11].
• With high quality samples, mRNA and protein levels for synapsin II and NSF were measured by real-time polymerase chain reaction and by immunoblotting [11].

Analytical, diagnostic and therapeutic context of SYN2

• We recently reported positive association of synapsin II with schizophrenia in a case-control study (Chen et al. 2004) [5].
• RESULTS: Although there was no significant difference in the genotypic distributions and allelic frequencies of either SYN2 or CPLX2 polymorphisms between the schizophrenia and control groups, the two-way haplotype analyses revealed significant associations with the disease (P < 0.05 after Bonferroni correction) [9].

References