Human SNAP25 ELISA KIT

Background: Established psychosocial risk factors increase the risk for experimentation among Mexican origin youth. Now, we comprehensively investigate the added contribution of select polymorphisms in candidate genetic pathways associated with sensation seeking, risk taking, and smoking phenotypes to predict experimentation. Methods: Participants (N = 1,118 Mexican origin youth) recruited from a large population-based cohort study in Houston, TX, provided prospective data on cigarette experimentation over 3 years. Psychosocial data were elicited twice-baseline and final follow-up. Participants were genotyped for 672 functional and tagging variants in the dopamine, serotonin, and opioid pathways. Results: After adjusting for gender and age, with a Bayesian False Discovery Probability set at 0.8 and prior probability of 0.05, six gene variants were significantly associated with risk of experimentation. After controlling for established risk factors, multivariable analyses revealed that participants with six or more risk alleles were 2.25 [95% confidence interval (CI), 1.62-3.13] times more likely to have experimented since baseline than participants with five or fewer. Among committed never-smokers (N = 872), three genes (OPRM1, SNAP25, HTR1B) were associated with experimentation as were all psychosocial factors. Among susceptible youth (N 246), older age at baseline, living with a smoker, and three different genes (HTR2A, DRD2, SLC6A3) predicted experimentation. Conclusions: Our findings, which have implications for development of culturally specific interventions, need to be validated in other ethnic groups. Impact: These results suggest that variations in select genes interact with a cognitive predisposition toward smoking. In susceptible adolescents, the impact of the genetic variants appears to be larger than committed never-smokers. Cancer Epidemiol Biomarkers Prev; 21(1); 228-38. (C) 2011 AACR.

It is generally accepted that information about some of the odorants in the natal streams of anadromous Pacific salmon (Genus Oncorhynchus) is imprinted during their seaward migration, and that anadromous Pacific salmon use olfaction to identify their natal streams during the homeward migration. However, little is known about the molecular mechanisms of the various pre-synaptic functions that are important for olfactory imprinting and memory retrieval in the salmon brain. Synaptosome-associated protein-25 (SNAP-25) mediates pre-synaptic vesicle exocytosis and regulates synaptic transmission and neuronal plasticity. Despite the importance of synaptic plasticity for memorization, the expression of SNAP-25 in the salmon brain is not well understood. In this study, snap25 expression was detected in chum salmon (O. keta) brains using molecular biological techniques. Two cDNAs encoding salmon SNAP-25 were isolated and sequenced (SNAP-25a and SNAP-25b). These cDNAs encoded proteins with 204 amino acid residues, which showed marked homology with each other (97%). The protein and nucleotide sequences demonstrated a high level of homology between salmon SNAP-25s and those of other teleost species. By quantitative PCR, the expression of snap25a and snap25b was detected in all regions of the salmon brain, especially in the telencephalon. The expression levels of snap25a in the olfactory blub were higher during seaward migration than in upriver and post-upriver migrations, reflecting synaptogenesis in the olfactory nervous system, and snap25b in the telencephalon was increased during upriver period. Our results indicated that snap25s gene is involved in synaptic plasticity for olfactory imprinting and/or olfactory memory retrieval in Pacific salmon.