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Human Polyclonal DTNBP1 Primary Antibody für IHC, IHC (p) - ABIN4306530
Gokhale, Mullin, Zlatic, Easley, Merritt, Raj, Larimore, Gordon, Peden, Sanyal, Faundez: The N-ethylmaleimide-sensitive factor and dysbindin interact to modulate synaptic plasticity. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2015
Show all 2 Pubmed References
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 (zeige RCC1 Antikörper) is a neurotoxin and whose depletion constitutes a micronutrient deficiency.
Loss-of-function alleles of dysbindin or Blos1 (zeige BLOC1S1 Antikörper) 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
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
Our results suggest that DTNBP1 and NRN1 (zeige NRN1 Antikörper) 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 (zeige GRIN1 Antikörper) 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 (zeige BLOC1S1 Antikörper) complex; this effect may lead to cognitive impairment.
This study demonstrated that BDNF (zeige BDNF Antikörper) 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 (zeige COMT Antikörper), BDNF (zeige BDNF Antikörper), 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)
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 (zeige NFKB1 Antikörper) activity to promote the expression of MMP-9 (zeige MMP9 Antikörper) and TNF-alpha (zeige TNF Antikörper)
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.
Nuclear SREBP1 (zeige SREBF1 Antikörper) is dramatically reduced in dysbindin-1 knockout mice.
loss of DTNBP1 in pyramidal neurons diminished activity-dependent secretion of brain-derived neurotrophic factor (BDNF (zeige BDNF Antikörper)).
Dysbindin-1 modulates thus D2 and D3 receptor (zeige DRD3 Antikörper) 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 (zeige DISC1 Antikörper) was partially reversed by coexpression of dysbindin.
dysbindin-1C, rather than dysbindin-1A, regulates adult hippocampal neurogenesis in a non-cell autonomous manner
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