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Dysbindin levels regulate the access to EGTA-sensitive vesicles at the neuromuscular junction.
Results indicate that perturbations downstream of DTNBP1, confer susceptibility to copper, a metal that in excess is a neurotoxin and whose depletion constitutes a micronutrient deficiency.
Loss-of-function alleles of dysbindin or Blos1 impaired neurotransmitter release and synaptic function and plasticity.
optimal binding ratio between Dysb and Ebony might contribute to such non-linear effects. Thus, Ddysb-dependent regulation of Ebony could be one of the mechanisms that mediate dopamine signal
Ddysb regulates glutamatergic transmission through its neuronal function and regulates dopamine metabolism by regulating Ebony expression in glial cells
study found that dysbindin (CG6856) is required presynaptically for the retrograde, homeostatic modulation of neurotransmission, and functions in a dose-dependent manner downstream or independently of calcium influx
Three investigated SNPs were rs165599, rs3737597, and rs1047631 of COMT, DISC1, and DTNBP1, respectively. Our results suggested that rs3737597 showed a significant association with schizophrenia in Europeans (odds ratio: 1.584, P: 0.002, 95% confidence interval: 1.176-2.134) under a random-effect framework. No other associations were found.
Multilevel ex vivo and in vivo analyses in postmortem brains demonstrate that interaction between antipsychotics and dysbindin-1 is mediated by an imbalance between the short and long isoforms of dopamine D2 receptors, leading to enhanced presynaptic D2 function within the prefrontal cortex.
Our results suggest that DTNBP1 and NRN1 genes show a joint effect on the risk for schizophrenia spectrum disorders. Although the precise mechanism underlying this effect is unclear, the fact that these genes have been involved in synaptic maturation, connectivity and glutamate signalling suggests that our findings could be of value as a link to the schizophrenia aetiology.
Study analyzed human-specific dysbindin-1B expression in multiple brain areas in mouse models and showed that dysbindin-1B exerts a dominant-negative effect on the BLOC-1 complex; this effect may lead to cognitive impairment.
This study demonstrated that BDNF and dysbindin-1 linked to risk for schizophrenia function together to regulate interneuron development and cortical network activity.
This is the first study to suggest that known and newly described polymorphisms in COMT, BDNF, and DTNBP1, genes associated with executive and memory functions in healthy individuals and other clinical populations may modulate cognitive outcome in patients with brain tumors
Data suggest that, in cardiomyocytes, TRIM32 attenuates activation of SRF signaling and hypertrophy due to dysbindin; TRIM24 promotes these effects. TRIM32 promotes dysbindin degradation; TRIM24 protects dysbindin from degradation. (TRIM = tripartite motif-containing protein; SRF = serum response factor)
In schizophrenia patients, there was a significant association of the rs909706 polymorphism with attention and a nonsignificant trend for set-shifting. The other SNPs and haplotypes were not associated with cognitive function.
Authors report the examination of DNA methylation status of DTNBP1 promoter region, one of the most credible candidate genes affected in SCZ.
DTNBP1 is likely to play a role in development of auditory related, visual and olfactory hallucinations
dysbindin-1A protein levels are highly regulated in the nucleus and that dysbindin-1A regulates transcription factor NF-kappa B activity to promote the expression of MMP-9 and TNF-alpha
Study demonstrated that dysbindin-1B, rather than dysbindin-1A and dysbindin-1C, has the ability to aggregate
The present findings intransgenic mice expressing human DTNBP1 support the role of dysbindin-1 in psychiatric disorders.
rs3213207 polymorphism may contribute to methamphetamine-induced panic disorder
Findings add further evidence suggesting an association between dysbindin gene variability and cognitive abnormalities in schizophrenia.
dysbindin-1 formed a protein complex with HDAC3 in human neuroblastoma cells
DISC1 forms a complex with dysbindin and increases its stability in association with a reduction in ubiquitylation.
In homozygotes and heterozygotes of risk allele (CC) of DTNBP1, there was a trend to volumetric reductions in brain regions, regardless of schizophrenia diagnosis.
loss of function mutations in the genes encoding dysbindin and its interacting BLOC-1 subunits
These data confirm at the level of mouse working memory and human working memory-associated physiology a genetic interaction between COMT and DTNBP1.
Multilevel ex vivo and in vivo analyses in genetically modified mice demonstrate that interaction between antipsychotics and dysbindin-1 is mediated by an imbalance between the short and long isoforms of dopamine D2 receptors, leading to enhanced presynaptic D2 function within the prefrontal cortex.
Nuclear SREBP1 is dramatically reduced in dysbindin-1 knockout mice.
loss of DTNBP1 in pyramidal neurons diminished activity-dependent secretion of brain-derived neurotrophic factor (BDNF).
Dysbindin-1 modulates thus D2 and D3 receptor signaling, supporting a link to schizophrenia
Results suggest that Dtnbp1 deficiency may lead to increased vulnerability to schizophrenia under environmental conditions where circadian rhythms are altered
Snapin-dysbindin interaction regulates synaptic vesicle positional priming through BLOC-1/AP-3-dependent sorting.
Dysbindin has three isoforms associating with different complexes in the P2 fraction of mouse brain.
Dysbindin-1C deficiency causes impaired autophagy, which is likely implicated in the pathogenesis of schizophrenia.
The neurite outgrowth defect induced by knockdown of DISC1 was partially reversed by coexpression of dysbindin.
dysbindin-1C, rather than dysbindin-1A, regulates adult hippocampal neurogenesis in a non-cell autonomous manner
Mecp2 regulates the expression of components belonging to the dysbindin interactome
the results of this study indicated that a loss of dysbindin-1 impairs hippocampal plasticity which may, in part, explain the role dysbindin-1 plays in the cognitive impairments of schizophrenia.
Loss of dysbindin led to enhanced CA3-CA1 AMPAR-mediated synaptic transmission and long term plasticity in hippocampal slices.
a novel cardiac role of Dysbindin in the activation of RhoA-SRF and MEK1-ERK1 signaling pathways and in the induction of cardiac hypertrophy, is reported.
This study demonistrated that the dysbindin-1 null mice show decreases in the [Ca(2+)]i,expression of L- and N-type Ca(2+)channels and several proteins involved in synaptic vesicle trafficking and priming.
Dys-/- mice exhibited increased compulsive and impulsive behaviors compared to control littermates suggesting the inability to suppress incorrectly-timed responses underlies their increased time to acquisition.
dysbindin and its associated complex sort cargoes from cell bodies to the synapse.
This gene encodes a protein that may play a role in organelle biogenesis associated with melanosomes, platelet dense granules, and lysosomes. A similar protein in mouse is a component of a protein complex termed biogenesis of lysosome-related organelles complex 1 (BLOC-1), and binds to alpha- and beta-dystrobrevins, which are components of the dystrophin-associated protein complex (DPC). Mutations in this gene are associated with Hermansky-Pudlak syndrome type 7. This gene may also be associated with schizophrenia. Multiple transcript variants encoding distinct isoforms have been identified for this gene.
, BLOC-1 subunit 8-A
, biogenesis of lysosome-related organelles complex 1 subunit 8-A
, dystrobrevin binding protein 1
, dystrobrevin-binding protein 1-A
, BLOC-1 subunit 8
, Hermansky-Pudlak syndrome 7 protein
, biogenesis of lysosomal organelles complex-1, subunit 8
, biogenesis of lysosome-related organelles complex 1 subunit 8
, HPS7 protein homolog
, dystrobrevin-binding protein 1
, hermansky-Pudlak syndrome 7 protein homolog
, distrobrevin binding protein 1