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Specific alleles of the SNAP25 (a synaptosome protein coding gene) were found to be significantly associated with Attention-Deficit Hyperactivity Disorder in more than 70% of the studies.
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Comparing clinical features of reported patients with SNAP25 mutations, the current patients demonstrated apparently milder clinical features with normal intelligence, and no magnetic resonance imaging abnormality or facial dysmorphism. Our results expand the clinical spectrum of SNAP25 mutations.
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report some evidence supporting the association of SNAP25 to Attention Deficit/Hyperactivity Disorder
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Single nucleotide polymorphism in SNAP-25 gene is associated with Attention deficit hyperactivity disorder.
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nine ADHD candidate single nucleotide polymorphisms (SNPs) in seven genes were tested for association with PD in 5333 cases and 12,019 healthy controls. No significant association was observed.
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Findings indicate that lower SNAP-25 in ventromedial caudate in schizophrenia is primarily due to less SNAP-25A, and that the remaining SNAP-25 is associated with greater protein-protein interaction with syntaxin. The absence of a link to recent treatment effects in the human samples, or to administration of antipsychotic drugs in rats suggests the findings are illness- and not treatment-related.
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Allelic variation of SNAP25 modulates development and plasticity of the prefrontal-limbic network and a shared genetic vulnerability between Bipolar Disorder and Schizophrenia.
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SH3BP5, LMO3, and SNAP25 were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.
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show that FOXC1 regulates the expression of RAB3GAP1, RAB3GAP2 and SNAP25
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The results of this study suggested that the polymorphisms rs3746544 and rs1051312 may increase the odds of developing ADHD.
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study demonstrated that miR-27a and -b, which are widely expressed in host cells, suppress SNAP25 and TXN2 expression through posttranscriptional gene silencing.
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Data suggest that A-syn (alpha-synuclein) promotes SNARE-dependent vesicle docking; phosphatidylserine (PS) removal from t-SNARE-bearing vesicles causes A-syn to inhibit vesicle docking; PS removal from v-SNARE-bearing vesicles promotes vesicle docking; the C-terminal 45 residues of A-syn are required for promotion of vesicle docking. (Here, t-SNARE is SNAP-25; v-SNARE is VAMP2.)
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our data indicate that the expression of SNAP25 is crucial for dendrite formation and is associated with the effects of targeted chemotherapy. The detection of SNAP25 expression in MB cells may thus be essential for the chemotherapeutic application of Ara-C.
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Robust association of the rs3746544 SNP and ASD, in both allele and haplotype-based analyses, was observed in Iranian population.
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Our results will provide novel evidence to reveal the possible role of SNAP-25 in B[a]P-induced neurotoxicity and may be helpful for searching the potential strategy for the prevention measures against B[a]P neurotoxicity.
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Our analysis indicated that there is no significant association between none of studied variants in SNAP-25 and ADHD.
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These results of this study suggested that SNAP25 and NOS1 genotypes influence ADHD symptoms only in adults with ADHD.
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Snap25 rs363050 (G) allele, which results in a reduced expression of Snap25, is associated with altered glycemic parameters in T2DM possibly because of reduced functionality in the exocytotic machinery leading to suboptimal release of insulin.
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single nucleotide polymorphisms in either the region of NEUROD6 or SNAP25 were significantly associated with Alzheimer's Disease, in APOE4+ females and APOE4+ males, respectively.
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Data demonstrate a role for SNAP-25 in controlling PSD-95 clustering and open the possibility that genetic reductions of the protein levels may contribute to the pathology through an effect on postsynaptic function and plasticity.
