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2 ctional roles of the three major isoforms of dysbindin-1, (A, B, and C) remain unknown, we generated
3 an hippocampal formations revealed that both dysbindin-1 and snapin are concentrated in tissue enrich
4 trophysiological deficits related to reduced dysbindin-1 and the potential role of PV cells, we exami
9 tions in the gene encoding the novel protein dysbindin-1 (DTNBP1) are among the most commonly reporte
11 ne-protein phosphatase-alpha (RPTPalpha) and dysbindin-1, each of which reduces Src activity via prot
13 ion of this gene and of its encoded protein, dysbindin-1, have been reported in the brains of schizop
20 nding, immunoelectron microscopy showed that dysbindin-1 is located in (i) synaptic vesicles of axosp
21 et al. show that, contrary to expectations, dysbindin-1 is located presynaptically in glutamatergic
22 oded protein dystrobrevin-binding protein 1 (dysbindin-1) is often reduced in excitatory cortical lim
23 ound between case-control differences in any dysbindin-1 isoform and the case-control differences in
24 ver, if the protein reductions encompass all dysbindin-1 isoforms or if they are associated with decr
27 izophrenia populations displayed presynaptic dysbindin-1 reductions averaging 18-42% (P = 0.027-0.000
28 bindin-1C and known post-synaptic effects of dysbindin-1 reductions in the rodent equivalent of the D
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