Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pharmacological actions of methamphetamine (METH) and phencyclidine (PCP) are different, but both of them can induce similar psychiatric disorders including abuse, intoxication, withdrawal, and psychotic symptoms like those of schizophrenia. These mental disorders are caused not only by their direct pharmacological effects, but also by secondary brain damage containing gene expression changes. In order to broadly grasp these alterations, we used serial analysis of gene expression (SAGE), a transcriptome analysis. We analyzed three cDNA libraries from cerebral cortices of saline (1 mL/kg)-, METH (4 mg/kg)-, or PCP (10 mg/kg)-treated Wistar rats (one hour after i.p. administration). The numbers of total tags were about 50,000 in each library, and approximately 18,000 kinds of tags were identified respectively. From the comparisons of three groups, we found both METH- and PCP-reactive genes. Upregulated genes contained calmodulin 2, stromal cell-derived factor receptor 1, brain-specific angiogenesis inhibitor 1-associated protein 2, ras homologue enriched in brain, basigin and thyrotropin-releasing hormone receptor. Downregulated genes contained lipocalin 2, aldolase A, importin 13, fatty acid binding protein 3, and glycine receptor alpha2 subunit. These data suggest important clues of common molecular basis in METH- and PCP-related psychiatric disorders.
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PMID:Serial analysis of gene expression in methamphetamine- and phencyclidine-treated rodent cerebral cortices: are there common mechanisms? 1554

A previous study revealed a number of methamphetamine (METH) and phencyclidine (PCP)-reactive tags in a rat brain through serial analysis of gene expression. The present study extends this previous study by investigating whether two genes, which deduced from METH/PCP-reactive tags, were identified as those encoding human transmembrane proteins of the immunoglobulin (Ig) superfamily, neuroplastin (NPTN) and basigin (BSG), confer genetic susceptibility to schizophrenia by analyzing single nucleotide polymorphisms (SNPs). There were nominally significant differences between the two groups in their allelic frequencies (T Ins/Del, chi2=4.910, d.f.=1, P=0.040) and genotypic distributions (T/T or T/Del, chi2=5.116, d.f.=1, P=0.036) of rs3840846 in the 5'-upstream of NPTN. The two groups differed significantly also in their allelic frequencies (G/T, chi2=4.229, d.f.=1, P=0.044), but not genotypic distributions of rs3743500 in the 5'-upstream of NPTN. The haplotypes constructed from the three SNPs (rs3840846, rs3826047 and rs3743500, in order) in the 5'-upstream of NPTN showed a significant association with schizophrenia (permutation P=0.036), in that T-G-T (permutation P=0.028) and del-G-G (permutation P=0.040) were under-represented and over-represented, respectively, in schizophrenia. A reporter construct driven by the 5'-upstream region containing any haplotype consisting of the three SNPs had substantial transcriptional activity. Notably, a reporter construct containing a haplotype T-G-T had significantly lower transcriptional activity as compared with one having a haplotype T-G-G or T-A-G. There was no significant difference between the two groups regarding allelic frequencies, genotypic distribution or the adopted SNP-combinatory haplotype for BSG. These results suggest that NPTN may be involved in genetic susceptibility to schizophrenia.
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PMID:Association study of putative promoter polymorphisms in the neuroplastin gene and schizophrenia. 1712 23