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1 ctor dysbindin, which is encoded by the gene DTNBP1.
2 ntity of the disease-associated haplotype at DTNBP1.
3 xpression of dystrobrevin binding protein 1 (DTNBP1), a well-supported susceptibility gene for schizo
4 tation reducing expression of either COMT or DTNBP1 alone produced working memory advantages, while,
5 of-function mutations in two of these genes, DTNBP1 and BLOC1S3, cause Hermansky-Pudlak syndrome, a h
6 cus on the schizophrenia susceptibility gene DTNBP1 and its product dysbindin, a subunit of the BLOC-
8 est known as dystrobrevin-binding protein 1 (DTNBP1) and may thus be associated with the dystrophin g
12 gene encoding the novel protein dysbindin-1 (DTNBP1) are among the most commonly reported genetic var
13 ly, the weight of evidence supports NRG1 and DTNBP1 as schizophrenia susceptibility loci, though work
14 International HapMap Project (HapMap), about DTNBP1 by specifically typing all associated single-nucl
16 eam of the schizophrenia susceptibility gene DTNBP1 confer susceptibility to copper, a metal that in
19 leotide polymorphisms within the 140-kb gene DTNBP1 (dystrobrevin-binding protein 1, or dysbindin) ar
20 ibility gene dystrobrevin-binding protein 1 (DTNBP1) encodes dysbindin, which along with its binding
21 ndin protein owing to a deletion in the gene Dtnbp1 (encoding dysbindin) and that mutation of the hum
23 nome-wide suggestive evidence for linkage of DTNBP1 expression to chromosome 8p, suggesting a locus t
24 of white European ancestry also index lower DTNBP1 expression, whereas putative 'protective' haploty
30 cytoskeleton organisation (ACTR3, CDC42BPA, DTNBP1, FERMT2, PRKCZ, RAC1), and cytokine production (F
32 nt genes (APOE, COMT, DAO, DRD1, DRD2, DRD4, DTNBP1, GABRB2, GRIN2B, HP, IL1B, MTHFR, PLXNA2, SLC6A4,
33 as well as ADCYAP1, BDNF, CNR1, COMT, DRD2, DTNBP1, GAD1, GRIA1, GRIN2B, HTR2A, NRG1, RELN, SNAP-25,
36 provides further evidence for a role of the DTNBP1 gene in the genetic etiology of schizophrenia.
41 bindin (dys; dystrobrevin-binding protein 1 (DTNBP1))--implicated through different mechanisms in cor
42 e reported confirmation of an association to DTNBP1 in independent European samples; however, reporte
45 by mutations in the schizophrenia risk gene Dtnbp1 led to spine deficiency, dysconnectivity in the e
46 wide significant evidence for linkage at the DTNBP1 locus on chromosome 6p22, and demonstrated that t
48 tiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophren
49 schizophrenia-susceptibility gene dysbindin (DTNBP1 on 6p22.3) encodes a neuronal protein that binds
50 sm for pathogenesis in which risk alleles in DTNBP1, or other factors that also downregulate dysbindi
51 e genes that regulate melanosome biogenesis (Dtnbp1, Pldn, Vps33a) also result in increased cis-plati
52 authors tested for an association between a DTNBP1 risk haplotype and a lifetime history of negative
53 issue samples and in the absence of the only DTNBP1 risk haplotype for schizophrenia reported in the
57 We studied the effects of transfection of DTNBP1 siRNA on cell surface levels of dopamine D2 recep
58 schizophrenia candidate genes (RGS4, DISC1, DTNBP1, STX7, TAAR6, PPP3CC, NRG1, DRD2, HTR2A, DAOA, AK
59 interacts with the fly homolog of Dysbindin (DTNBP1) via direct protein-protein interaction in develo
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