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1  in myoblasts resulted in elevated levels of dysbindin.
2 g proteins, Pallidin, Muted, Cappuccino, and Dysbindin.
3 ne encoding the dystrobrevin-binding protein dysbindin.
4 ic mutations in a schizophrenia risk factor, dysbindin.
5 dentified RhoA as a novel binding partner of Dysbindin.
6 tions in the gene encoding the novel protein dysbindin-1 (DTNBP1) are among the most commonly reporte
7                                 The gene for dysbindin-1 (DTNBP1) is located at 6p and has also been
8 an hippocampal formations revealed that both dysbindin-1 and snapin are concentrated in tissue enrich
9 trophysiological deficits related to reduced dysbindin-1 and the potential role of PV cells, we exami
10                           Further studies of dysbindin-1 and the proteins with which it interacts can
11 ucleotide polymorphisms in the gene encoding dysbindin-1 at 6p22.3.
12                                              Dysbindin-1 disruption altered dopamine-related behavior
13                            The gene encoding dysbindin-1 has recently been implicated in susceptibili
14 ric diagnoses, suggesting a general role for dysbindin-1 in cognition.
15                   In contrast to the role of dysbindin-1 in glutamatergic transmission, gamma-band ab
16                        We found that reduced dysbindin-1 in mice yielded deficits in auditory-evoked
17                              The function of dysbindin-1 in presynaptic, postsynaptic and microtubule
18 ate here that snapin is a binding partner of dysbindin-1 in vitro and in the brain.
19                                              Dysbindin-1 is best known as dystrobrevin-binding protei
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 ound between case-control differences in any dysbindin-1 isoform and the case-control differences in
23 ver, if the protein reductions encompass all dysbindin-1 isoforms or if they are associated with decr
24                                          How dysbindin-1 might affect glutamate release nevertheless
25 and novel object recognition are impaired in dysbindin-1 null mice.
26                                   We studied dysbindin-1 null mutant mice (Dys(-/-)) to shed light on
27 axon terminal loss or neuroleptic effects on dysbindin-1 or VGluT-1.
28 s of the DTBPN1 gene associated with reduced dysbindin-1 protein (Dys) expression negatively impact c
29 izophrenia populations displayed presynaptic dysbindin-1 reductions averaging 18-42% (P = 0.027-0.000
30 bindin-1C and known post-synaptic effects of dysbindin-1 reductions in the rodent equivalent of the D
31       Our findings indicate that presynaptic dysbindin-1 reductions independent of the dystrophin gly
32                                              Dysbindin-1 regulates D2-receptor trafficking and is imp
33       The dominant circuit impact of reduced dysbindin-1 was impaired inhibition, and PV cell immunor
34 oded protein dystrobrevin-binding protein 1 (dysbindin-1) is often reduced in excitatory cortical lim
35 ctional roles of the three major isoforms of dysbindin-1, (A, B, and C) remain unknown, we generated
36                           Here, we show that dysbindin-1, a protein decreased in the brain of individ
37                                              Dysbindin-1, a protein that regulates aspects of early a
38 ne-protein phosphatase-alpha (RPTPalpha) and dysbindin-1, each of which reduces Src activity via prot
39 ion of this gene and of its encoded protein, dysbindin-1, have been reported in the brains of schizop
40                               We explored in dysbindin-1-deficient mice (dys-/-) (1) schizophrenia-re
41 t mouse, dys-1A(-/-), with selective loss of dysbindin-1A and investigated schizophrenia-related phen
42 icant reductions in dysbindin-1C (but not in dysbindin-1A or -1B) in schizophrenia (P = 0.022).
43                                      Loss of dysbindin-1A resulted in heightened initial exploration
44 idence for differential functional roles for dysbindin-1A vs dysbindin-1C isoforms among phenotypes r
45                                      Loss of dysbindin-1A was not associated with disruption of eithe
46 ing DISC1 (disrupted in schizophrenia 1) and dysbindin-1B are found in insoluble forms within brain h
47 x (DLPFC) revealed significant reductions in dysbindin-1C (but not in dysbindin-1A or -1B) in schizop
48  predominantly post-synaptic localization of dysbindin-1C and known post-synaptic effects of dysbindi
49  mRNA translation and/or processes promoting dysbindin-1C degradation (e.g. oxidative stress, phospho
50  the present findings suggest that decreased dysbindin-1C in the DLPFC may contribute to the cognitiv
51 rential functional roles for dysbindin-1A vs dysbindin-1C isoforms among phenotypes relevant to the p
52       Consequently, the mean 60% decrease in dysbindin-1C observed in 71% of our case-control pairs a
53 ed a concomitant change in the expression of dysbindin-1C.
54 structural homologue of the acidic domain of dysbindin, a component of the dystrophin-associated prot
55 teins and identified a critical function for dysbindin, a gene linked to schizophrenia in humans.
56 is screen identified a critical function for dysbindin, a gene linked to schizophrenia in humans.
57 we found that TRIM32 binds and ubiquitinates dysbindin, a protein implicated in the genetic aetiology
58 itive to genetic defects in a locus encoding dysbindin, a protein required for synapse biology and im
59                              Last, levels of dysbindin, a regulator of the membrane availability of d
60  evidence that thin controls release through dysbindin, a schizophrenia-susceptibility gene required
61                           Here, we show that dysbindin, a schizophrenia-susceptibility gene widely ex
62 genes encoding the schizophrenia risk factor dysbindin, a subunit of the biogenesis of lysosome-relat
63 a susceptibility gene DTNBP1 and its product dysbindin, a subunit of the BLOC-1 complex, and describe
64 t of late endosomes (LEs) and interacts with dysbindin, a subunit of the endosomal sorting complex BL
65 schizophrenia, but little is known about how dysbindin affects neuronal function in the circuitry und
66 promote dysbindin decay but rather protected dysbindin against degradation by TRIM32.
67           We found 491 proteins sensitive to dysbindin and BLOC-1 loss of function.
68 otrusions, and reveal the essential roles of dysbindin and CaMKIIalpha in the stabilization of dendri
69   Our data identify TRIM32 as a regulator of dysbindin and demonstrate that the LGMD2H/STM mutations
70 echanism of post-translational regulation of dysbindin and hypertrophy via TRIM24 and TRIM32 and show
71 hermore, the D487N mutant could bind to both dysbindin and its E2 enzyme but was defective in monoubi
72  of function mutations in the genes encoding dysbindin and its interacting BLOC-1 subunits.
73 echanisms controlling the cellular levels of dysbindin and its interacting partners may participate i
74 These data suggest that the acidic domain of dysbindin and its paralogs in humans may function to rec
75 94H impair ubiquitin ligase activity towards dysbindin and were mislocalized in heterologous cells.
76 g to a deletion in the gene Dtnbp1 (encoding dysbindin) and that mutation of the human ortholog DTNBP
77 enia, including the DISC1, COMT, neuregulin, dysbindin, and alpha-7 nicotinic receptor genes, appear
78    Furthermore, we demonstrated that Arp2/3, dysbindin, and subunits of the BLOC-1 complex biochemica
79 e DTNBP1 (dystrobrevin-binding protein 1, or dysbindin) are strongly associated with schizophrenia.
80 ow performed a yeast two-hybrid screen using dysbindin as bait against a cardiac cDNA library to iden
81                                              Dysbindin assembles into the biogenesis of lysosome-rela
82                                              Dysbindin/BLOC-1 and ATP7A genetically and biochemically
83                                        Human dysbindin/BLOC-1 coprecipitates with NSF and vice versa,
84 fusion machinery as factors downregulated in dysbindin/BLOC-1 deficiency in neuroectodermal cells and
85                 Our results demonstrate that dysbindin/BLOC-1 expression defects result in altered ce
86 tides whose cellular content is sensitive to dysbindin/BLOC-1 loss of function.
87                                              Dysbindin/BLOC-1 loss-of-function alleles do not affect
88          To test the hypothesis that NSF and dysbindin/BLOC-1 participate in a pathway-regulating syn
89 ein networks, or interactomes, downstream of dysbindin/BLOC-1 remain partially explored despite their
90 ic function, we examined the role for NSF in dysbindin/BLOC-1-dependent synaptic homeostatic plastici
91  and dependent factors in the hippocampus of dysbindin/BLOC-1-null mice.
92 ouse null alleles muted (Bloc1s5(mu/mu)) and dysbindin (Bloc1s8(sdy/sdy)).
93 n of the schizophrenia susceptibility factor dysbindin (Bloc1s8) or two other dysbindin-interacting p
94               In addition, mutation of human Dysbindin causes HPS type 7.
95 BP1, or other factors that also downregulate dysbindin, compromise the ability of BLOC-1 to traffic D
96                                        Thus, dysbindin controls hippocampal LTP by selective regulati
97 urprisingly, however, TRIM24 did not promote dysbindin decay but rather protected dysbindin against d
98  polymerization complex Arp2/3 is reduced in dysbindin-deficient cells, thus affecting actin-dependen
99               However, mechanisms engaged by dysbindin defining schizophrenia susceptibility pathways
100                              Although intact dysbindin did not bind any CK1 isoform, deletion of its
101                       In contrast, decreased dysbindin did not change dopamine D1 receptor (DRD1) lev
102 B (cAMP response element-binding protein) in dysbindin downregulated cells, demonstrating enhanced in
103        The schizophrenia-susceptibility gene dysbindin (DTNBP1 on 6p22.3) encodes a neuronal protein
104 ptibility loci relates to the genes encoding dysbindin (DTNBP1) and neuregulin (NRG1).
105 the evidence to be strong are those encoding dysbindin (DTNBP1) and neuregulin 1 (NRG1).
106 nctionally interacts with the fly homolog of Dysbindin (DTNBP1) via direct protein-protein interactio
107 rder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-
108 es--catechol-O-methyl transferase (COMT) and dysbindin (dys; dystrobrevin-binding protein 1 (DTNBP1))
109 ons in the schizophrenia susceptibility gene dysbindin (dysb), in isolation or in combination with nu
110                        Little is known about dysbindin expression in normal or schizophrenic brain.
111                                              Dysbindin expression is reduced in schizophrenic brain t
112 rated an association between variants in the dysbindin gene (DTNBP1) and schizophrenia.
113 o determine whether genetic variation in the dysbindin gene affects cortical dysbindin mRNA levels.
114                            Disruption of the dysbindin gene dramatically increased NR2A-mediated syna
115                 Although no mutations in the dysbindin gene have been found, the recent identificatio
116 d neurons in mice carrying a deletion in the dysbindin gene have fewer dendritic spines.
117 ficient to rule out the possibility that the dysbindin gene is not the actual susceptibility gene, bu
118              Findings suggest that the human dysbindin gene may play a role in the susceptibility to
119                                Disruption of dysbindin gene resulted in a marked decrease in the exci
120     In each subject, 10 polymorphisms in the dysbindin gene were genotyped and assessed.
121 ied statistically significantly according to dysbindin genotype.
122 eduction of NSF alone or in combination with dysbindin haploinsufficiency impaired homeostatic synapt
123 g the HPS phenotype in humans, indicate that dysbindin has a role in the biogenesis of lysosome-relat
124                                              Dysbindin has been implicated in the pathogenesis of sch
125 o studies should examine the significance of Dysbindin in cardiomyopathy.
126 ant Sandy mice, we have explored the role of dysbindin in dopamine signaling and neuronal function in
127 istently, we found that TRIM32 also degraded dysbindin in neonatal rat ventricular cardiomyocytes as
128 ported earlier as an E3 ubiquitin ligase for dysbindin in skeletal muscle.
129  conclusion, we show a novel cardiac role of Dysbindin in the activation of RhoA-SRF and MEK1-ERK1 si
130 s has revealed reduced levels of the protein dysbindin in the brains of those suffering from the neur
131     These findings elucidate the function of dysbindin in the dynamic morphogenesis of dendritic prot
132 ithin presynaptic boutons, and Thin degrades Dysbindin in vitro.
133 d mechanistic characterization revealed that Dysbindin induced cardiac hypertrophy via RhoA-SRF and M
134 lity factor dysbindin (Bloc1s8) or two other dysbindin-interacting polypeptides, which assemble into
135 NA and protein levels of key components of a dysbindin interaction network by, quantitative real time
136 ed Ca(2+) sensor, we demonstrate that snapin-dysbindin interaction regulates SV positional priming th
137 he expression of components belonging to the dysbindin interactome and these molecular differences ma
138 cardiac cDNA library to identify the cardiac dysbindin interactome.
139 1 encodes a polypeptide that assembles, with dysbindin, into the octameric BLOC-1 complex.
140                            We also show that dysbindin is a component of the biogenesis of lysosome-r
141 ndent samples provides further evidence that dysbindin is a possible schizophrenia susceptibility gen
142                We have previously shown that dysbindin is a potent inducer of cardiomyocyte hypertrop
143                                              Dysbindin is a schizophrenia susceptibility factor and s
144                                              Dysbindin is a schizophrenia susceptibility gene require
145                                              Dysbindin is a ubiquitously expressed protein that binds
146                                              Dysbindin is an established schizophrenia susceptibility
147          These data add to the evidence that dysbindin is an etiologic factor in schizophrenia risk.
148                                        Thus, dysbindin is essential for adaptive neural plasticity an
149                                      Because Dysbindin is highly expressed in the heart, we aimed her
150                                We found that dysbindin is required presynaptically for the retrograde
151                        Our results show that dysbindin is required to stabilize dendritic protrusions
152    We conclude that further investigation of dysbindin is warranted.
153                    The DTNBP1 gene, encoding dysbindin, is now generally considered to be a susceptib
154                                      Using a dysbindin knockout line (dys(-/-)) derived from the natu
155                                     Thin and Dysbindin localize in proximity within presynaptic bouto
156                                       Hence, dysbindin might contribute to the spine pathology of sch
157                                              Dysbindin mRNA is expressed widely in the brain, and its
158 enia had statistically significantly reduced dysbindin mRNA levels in multiple layers of the dorsolat
159 ls in the dorsolateral prefrontal cortex and dysbindin mRNA levels in the midbrain by in situ hybridi
160                                 Variation in dysbindin mRNA levels may be determined in part by varia
161                                     Cortical dysbindin mRNA levels varied statistically significantly
162                                              Dysbindin mRNA levels were quantitatively reduced in the
163 ation in the dysbindin gene affects cortical dysbindin mRNA levels.
164                                              Dysbindin mRNA was detected in the frontal cortex, tempo
165                                         This dysbindin mutant phenotype is fully rescued by presynapt
166 out line (dys(-/-)) derived from the natural dysbindin mutant Sandy mice, we have explored the role o
167 ic risk factors for schizophrenia, including dysbindin, neuregulin 1, DAOA, COMT, and DISC1, and neur
168  PI4KIIalpha content in the dentate gyrus of dysbindin-null BLOC-1 deficiency and AP-3-null mice.
169 proteomics combined with genetic analyses in dysbindin-null mice (Mus musculus) and the genome of sch
170 ot NR2B, in hippocampal neurons derived from dysbindin-null mutant mice (Dys-/-).
171 he hyperactivity of dendritic protrusions in dysbindin-null neurons is attributed in part to decrease
172                                           In dysbindin-null neurons, dendritic protrusions are hypera
173  rescued by presynaptic expression of either dysbindin or Drosophila NSF.
174 fied a robust activation of SRF signaling by Dysbindin overexpression that was associated with signif
175 iously described, we found that mutations in dysbindin precluded homeostatic synaptic plasticity elic
176 ystems have shown that Snapin interacts with Dysbindin, prompting us to test whether Snapin might be
177  show that the sdy mutant mouse expresses no dysbindin protein owing to a deletion in the gene Dtnbp1
178                       DTNBP1 siRNA decreased dysbindin protein, increased cell surface DRD2 and block
179                            The expression of dysbindin proteins is decreased in the brains of schizop
180 eal subunit-specific regulation of NMDARs by dysbindin, providing an unexpected link between these tw
181                      Exogenous expression of dysbindin reduced NR2A surface expression in both wild-t
182   Taken together, these results suggest that dysbindin regulates PFC function by facilitating D2-medi
183          It has yet to be determined whether dysbindin regulates the dynamics of dendritic protrusion
184 henotypes in two cellular compartments where dysbindin resides, endosomes and presynapses.
185                      These results elucidate dysbindin's modulation of D2-related behavior, cortical
186 with schizophrenia and controls, we compared dysbindin, synaptophysin, spinophilin, and cyclophilin m
187 ia binding to the coiled coil domain protein Dysbindin, the delivery of Fas from endosomes to lysosom
188 rotein degradation-dependent proteostasis of Dysbindin to homeostatic regulation of neurotransmitter
189 ggests that snapin functions in concert with dysbindin to modulate vesicle release and possibly homeo
190 tion of SRF signaling and hypertrophy due to dysbindin, whereas TRIM24 promoted these effects in neon
191 trobrevin-binding protein 1 (DTNBP1) encodes dysbindin, which along with its binding partner Muted is
192                The authors hypothesized that dysbindin, which is a probable susceptibility gene for s
193 ning the schizophrenia susceptibility factor dysbindin, which is encoded by the gene DTNBP1.
194 d molecular mechanisms of the association of dysbindin with psychosis.

 
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