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Dysbindin

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https://www.readbyqxmd.com/read/28465353/trim24-promotes-while-trim32-inhibits-cardiomyocyte-hypertrophy-via-regulation-of-dysbindin-protein-levels
#1
Ankush Borlepawar, Ashraf Yusuf Rangrez, Alexander Bernt, Lynn Christen, Samuel Sossalla, Derk Frank, Norbert Frey
We have previously shown that Dysbindin is a potent inducer of cardiomyocyte hypertrophy via activation of Rho-dependent SRF signaling. We now performed a Yeast-two hybrid screen using Dysbindin as bait against a cardiac cDNA library to identify the cardiac Dysbindin interactome. Amongst several putative binding proteins, we identified Tripartite motif-containing protein 24 (TRIM24) and confirmed this interaction by co-immunoprecipitation and co-immunostaining. Another TRIM family protein, TRIM32 has earlier been reported as an E3 ubiquitin ligase for Dysbindin in skeletal muscle...
May 2, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28438837/an-unpredicted-aggregation-critical-region-of-the-actin-polymerizing-protein-triobp-1-tara-determined-by-elucidation-of-its-domain-structure
#2
Nicholas J Bradshaw, Antony S K Yerabham, Rita Marreiros, Tao Zhang, Luitgard Nagel-Steger, Carsten Korth
Protein aggregation resulting from disruptions in proteostasis in the brains of patients with chronic mental illness is an emerging theme particularly in the study of schizophrenia. For example, proteins such as Disrupted in Schizophrenia 1 (DISC1) and dysbindin-1B are present in insoluble aggregates, detectable within brain homogenates from such patients. Using an epitope discovery and proteomics approach to compare post-mortem brain samples from schizophrenia patients and controls, we recently identified TRIO-Binding Protein 1 (TRIOBP-1, also known as Tara) as another aggregation-associated protein...
April 24, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28344592/dysbindin-deficiency-modifies-the-expression-of-gaba-neuron-and-ion-permeation-transcripts-in-the-developing-hippocampus
#3
Jennifer Larimore, Stephanie A Zlatic, Miranda Arnold, Kaela S Singleton, Rebecca Cross, Hannah Rudolph, Martha V Bruegge, Andrea Sweetman, Cecilia Garza, Eli Whisnant, Victor Faundez
The neurodevelopmental factor dysbindin is required for synapse function and GABA interneuron development. Dysbindin protein levels are reduced in the hippocampus of schizophrenia patients. Mouse dysbindin genetic defects and other mouse models of neurodevelopmental disorders share defective GABAergic neurotransmission and, in several instances, a loss of parvalbumin-positive interneuron phenotypes. This suggests that mechanisms downstream of dysbindin deficiency, such as those affecting GABA interneurons, could inform pathways contributing to or ameliorating diverse neurodevelopmental disorders...
2017: Frontiers in Genetics
https://www.readbyqxmd.com/read/28317021/the-bloc-1-subunit-pallidin-facilitates-activity-dependent-synaptic-vesicle-recycling
#4
Xun Chen, Wenpei Ma, Shixing Zhang, Jeremy Paluch, Wanlin Guo, Dion K Dickman
Membrane trafficking pathways must be exquisitely coordinated at synaptic terminals to maintain functionality, particularly during conditions of high activity. We have generated null mutations in the Drosophila homolog of pallidin, a central subunit of the biogenesis of lysosome-related organelles complex-1 (BLOC-1), to determine its role in synaptic development and physiology. We find that Pallidin localizes to presynaptic microtubules and cytoskeletal structures, and that the stability of Pallidin protein is highly dependent on the BLOC-1 components Dysbindin and Blos1...
January 2017: ENeuro
https://www.readbyqxmd.com/read/28259707/clinical-and-molecular-phenotyping-of-a-child-with-hermansky-pudlak-syndrome-7-an-uncommon-genetic-type-of-hps
#5
Melanie M Bryan, Nathanial J Tolman, Karen L Simon, Marjan Huizing, Robert B Hufnagel, Brian P Brooks, Vladislav Speransky, James C Mullikin, William A Gahl, May Christine V Malicdan, Bernadette R Gochuico
PURPOSE: Hermansky-Pudlak syndrome (HPS) is a rare inherited disorder with ten reported genetic types; each type has defects in subunits of either Adaptor Protein-3 complex or Biogenesis of Lysosome-related Organelles Complex (BLOC)-1, -2, or -3. Very few patients with BLOC-1 deficiency (HPS-7, -8, and -9 types) have been diagnosed. We report results of comprehensive clinical testing and molecular analyses of primary fibroblasts from a new case of HPS-7. RESULTS: A 6-year old Paraguayan male presented with hypopigmentation, ocular albinism, nystagmus, reduced visual acuity, and easy bruising...
April 2017: Molecular Genetics and Metabolism
https://www.readbyqxmd.com/read/27986973/dysregulation-of-specialized-delay-interference-dependent-working-memory-following-loss-of-dysbindin-1a-in-schizophrenia-related-phenotypes
#6
Emilie I Petit, Zuzanna Michalak, Rachel Cox, Colm M P O'Tuathaigh, Niamh Clarke, Orna Tighe, Konrad Talbot, Derek Blake, Josephine Joel, Alexander Shaw, Steven A Sheardown, Alastair D Morrison, Stephen Wilson, Ellen M Shapland, David C Henshall, James N Kew, Brian P Kirby, John L Waddington
Dysbindin-1, a protein that regulates aspects of early and late brain development, has been implicated in the pathobiology of schizophrenia. As the functional roles of the three major isoforms of dysbindin-1, (A, B, and C) remain unknown, we generated a novel mutant mouse, dys-1A(-/-), with selective loss of dysbindin-1A and investigated schizophrenia-related phenotypes in both males and females. Loss of dysbindin-1A resulted in heightened initial exploration and disruption in subsequent habituation to a novel environment, together with heightened anxiety-related behavior in a stressful environment...
May 2017: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/27927957/the-proteome-of-bloc-1-genetic-defects-identifies-the-arp2-3-actin-polymerization-complex-to-function-downstream-of-the-schizophrenia-susceptibility-factor-dysbindin-at-the-synapse
#7
Avanti Gokhale, Cortnie Hartwig, Amanda H Freeman, Ravi Das, Stephanie A Zlatic, Rachel Vistein, Amelia Burch, Guillemette Carrot, Arielle F Lewis, Sheldon Nelms, Dion K Dickman, Manojkumar A Puthenveedu, Daniel N Cox, Victor Faundez
Proteome modifications downstream of monogenic or polygenic disorders have the potential to uncover novel molecular mechanisms participating in pathogenesis and/or extragenic modification of phenotypic expression. We tested this idea by determining the proteome sensitive to genetic defects in a locus encoding dysbindin, a protein required for synapse biology and implicated in schizophrenia risk. We applied quantitative mass spectrometry to identify proteins expressed in neuronal cells the abundance of which was altered after downregulation of the schizophrenia susceptibility factor dysbindin (Bloc1s8) or two other dysbindin-interacting polypeptides, which assemble into the octameric biogenesis of lysosome-related organelles complex 1 (BLOC-1)...
December 7, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27855309/evidence-of-an-epistatic-effect-between-dysbindin-1-and-neuritin-1-genes-on-the-risk-for-schizophrenia-spectrum-disorders
#8
C Prats, B Arias, J Moya-Higueras, E Pomarol-Clotet, M Parellada, A González-Pinto, V Peralta, M I Ibáñez, M Martín, L Fañanás, M Fatjó-Vilas
BACKGROUND: The interest in studying gene-gene interactions is increasing for psychiatric diseases such as schizophrenia-spectrum disorders (SSD), where multiple genes are involved. Dysbindin-1 (DTNBP1) and Neuritin-1 (NRN1) genes have been previously associated with SSD and both are involved in synaptic plasticity. We aimed to study whether these genes show an epistatic effect on the risk for SSD. METHODS: The sample comprised 388 SSD patients and 397 healthy subjects...
November 14, 2016: European Psychiatry: the Journal of the Association of European Psychiatrists
https://www.readbyqxmd.com/read/27713690/the-endosome-localized-arf-gap-agap1-modulates-dendritic-spine-morphology-downstream-of-the-neurodevelopmental-disorder-factor-dysbindin
#9
Miranda Arnold, Rebecca Cross, Kaela S Singleton, Stephanie Zlatic, Christopher Chapleau, Ariana P Mullin, Isaiah Rolle, Carlene C Moore, Anne Theibert, Lucas Pozzo-Miller, Victor Faundez, Jennifer Larimore
AGAP1 is an Arf1 GTPase activating protein that interacts with the vesicle-associated protein complexes adaptor protein 3 (AP-3) and Biogenesis of Lysosome Related Organelles Complex-1 (BLOC-1). Overexpression of AGAP1 in non-neuronal cells results in an accumulation of endosomal cargoes, which suggests a role in endosome-dependent traffic. In addition, AGAP1 is a candidate susceptibility gene for two neurodevelopmental disorders, autism spectrum disorder (ASD) and schizophrenia (SZ); yet its localization and function in neurons have not been described...
2016: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/27545194/visualization-of-disc1-dysbindin-interaction-in-glutamatergic-synaptic-termini-in-fruit-flies
#10
K Furukubo-Tokunaga, K Kurita, K Honjo, H Pandey, T Ando, K Takayama, Y Arai, H Mochizuki, M Ando, A Kamiya, A Sawa
No abstract text is available yet for this article.
September 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/27439747/effects-of-fingolimod-administration-in-a-genetic-model-of-cognitive-deficits
#11
D Becker-Krail, A Q Farrand, H A Boger, A Lavin
Notwithstanding recent advances, cognitive impairments are among the most difficult-to-treat symptoms in neuropsychiatric disorders. Deficits in information processing contributing to memory and sociability impairments are found across neuropsychiatric-related disorders. Previously, we have shown that mutations in the DTNBP1 gene (encoding dystrobrevin-binding protein 1 [dysbindin-1]) lead to abnormalities in synaptic glutamate release in the prefrontal cortex (PFC) and hippocampus and to cognitive deficits; glutamatergic transmission is important for cortical recurrent excitation that allows information processing in the PFC...
May 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/27421225/the-pathogenic-mechanism-of-dysbindin-1b-toxic-aggregation-bloc-1-and-intercellular-vesicle-trafficking
#12
Wei Yang, Chunyan Zhu, Yan Shen, Qi Xu
DTNBP1, which encodes dysbindin-1, is associated with cognitive impairment. Genetic evidence indicates that the C allele of rs117610176 leads to an increase in DTNBP-1b mRNA splicing in patients with paranoid schizophrenia. In addition, dysbindin-1B, rather than dysbindin-1A/C, exhibits a tendency toward toxic aggregation. In postmortem brains, dysbindin-1B not only aggregates with itself, it also co-aggregates with proteins that interact with it. However, the pathogenic mechanism underlying dysbindin-1B toxic aggregation remains unknown...
October 1, 2016: Neuroscience
https://www.readbyqxmd.com/read/27346367/interaction-between-disc1-and-chl1-in-regulation-of-neurite-outgrowth
#13
Jun Ren, Tian Zhao, Yiliang Xu, Haihong Ye
Disrupted-in-schizophrenia 1 (DISC1), a gene susceptible for major mental illnesses, including schizophrenia, plays multiple roles in neural development, including neuronal proliferation, maturation, migration and neurite outgrowth. DISC1 regulates neurite length via interaction with several intracellular proteins, such as NDEL1, FEZ1 and dysbindin. However, the signal transduction mechanism upstream of DISC1 in regulating neurite outgrowth remains to be elucidated. Here we show that DISC1 interacts with the intracellular domain of close homolog of L1 (CHL1), a member of the L1 family of neural cell adhesion molecules...
October 1, 2016: Brain Research
https://www.readbyqxmd.com/read/27281120/dysbindin-as-a-novel-biomarker-for-pancreatic-ductal-adenocarcinoma-identified-by-proteomic-profiling
#14
Xin Guo, Xiaohui Lv, Cheng Fang, Xing Lv, Fengsong Wang, Dongmei Wang, Jun Zhao, Yueyun Ma, Yu Xue, Quan Bai, Xuebiao Yao, Yong Chen
Pancreatic adenocarcinoma (PDAC) is known to have a poor prognosis partly because of lack of effective biomarkers. In the test set, we investigated dysbindin (DTNBP1) as a potential biomarker for PDAC by comparing preoperative and postoperative serum mass spectrometry (MS) proteomic profilings. Of the included 50 PDAC patients, 42 (positivity of 84.0%) detected a lower MS peak in postoperative serums than preoperative ones which was then identified as dysbindin. In the verification set, receiver operating characteristics (ROC) were used to assess diagnostic efficiency...
October 15, 2016: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/27231216/%C3%AE-taxilin-participates-in-differentiation-of-c2c12-myoblasts-into-myotubes
#15
Hiroshi Sakane, Tomohiko Makiyama, Satoru Nogami, Yukimi Horii, Kenji Akasaki, Hiromichi Shirataki
Myogenesis is required for the development of skeletal muscle. Accumulating evidence indicates that the expression of several genes are upregulated during myogenesis and these genes play pivotal roles in myogenesis. However, the molecular mechanism underlying myogenesis is not fully understood. In this study, we found that β-taxilin, which is specifically expressed in the skeletal muscle and heart tissues, was progressively expressed during differentiation of C2C12 myoblasts into myotubes, prompting us to investigate the role of β-taxilin in myogenesis...
July 15, 2016: Experimental Cell Research
https://www.readbyqxmd.com/read/27134685/effects-of-sex-and-dtnbp1-dysbindin-null-gene-mutation-on-the-developmental-glun2b-glun2a-switch-in-the-mouse-cortex-and-hippocampus
#16
Duncan Sinclair, Joseph Cesare, Mary McMullen, Greg C Carlson, Chang-Gyu Hahn, Karin E Borgmann-Winter
BACKGROUND: Neurodevelopmental disorders such as autism spectrum disorders and schizophrenia differentially impact males and females and are highly heritable. The ways in which sex and genetic vulnerability influence the pathogenesis of these disorders are not clearly understood. The n-methyl-d-aspartate (NMDA) receptor pathway has been implicated in schizophrenia and autism spectrum disorders and changes dramatically across postnatal development at the level of the GluN2B-GluN2A subunit "switch" (a shift from reliance on GluN2B-containing receptors to reliance on GluN2A-containing receptors)...
2016: Journal of Neurodevelopmental Disorders
https://www.readbyqxmd.com/read/27130439/schizophrenia-susceptibility-gene-product-dysbindin-1-regulates-the-homeostasis-of-cyclin-d1
#17
Hidenori Ito, Rika Morishita, Koh-Ichi Nagata
Dysbindin-1 (dystrobrevin binding protein-1, DTNBP1) is now widely accepted as a potential schizophrenia susceptibility gene and accumulating evidence indicates its functions in the neural development. In this study, we tried to identify new binding partners for dysbindin-1 to clarify the novel function of this molecule. When consulted with BioGRID protein interaction database, cyclin D3 was found to be a possible binding partner for dysbindin-1. We then examined the interaction between various dysbindin-1 isoforms (dysbindin-1A, -1B and -1C) and all three D-type cyclins (cyclin D1, D2, and D3) by immunoprecipitation with the COS7 cell expression system, and found that dysbindin-1A preferentially interacts with cyclin D1...
August 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/26976042/disc1-causes-associative-memory-and-neurodevelopmental-defects-in-fruit-flies
#18
K Furukubo-Tokunaga, K Kurita, K Honjo, H Pandey, T Ando, K Takayama, Y Arai, H Mochizuki, M Ando, A Kamiya, A Sawa
Originally found in a Scottish family with diverse mental disorders, the DISC1 protein has been characterized as an intracellular scaffold protein that associates with diverse binding partners in neural development. To explore its functions in a genetically tractable system, we expressed the human DISC1 in fruit flies (Drosophila melanogaster). As in mammalian neurons, DISC1 is localized to diverse subcellular domains of developing fly neurons including the nuclei, axons and dendrites. Overexpression of DISC1 impairs associative memory...
September 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/26873854/neuronal-activity-induced-sterol-regulatory-element-binding-protein-1-srebp1-is-disrupted-in-dysbindin-null-mice-potential-link-to-cognitive-impairment-in-schizophrenia
#19
Yong Chen, Sookhee Bang, Mary F McMullen, Hala Kazi, Konrad Talbot, Mei-Xuan Ho, Greg Carlson, Steven E Arnold, Wei-Yi Ong, Sangwon F Kim
Schizophrenia is a chronic debilitating neuropsychiatric disorder that affects about 1 % of the population. Dystrobrevin-binding protein 1 (DTNBP1 or dysbindin) is one of the Research Domain Constructs (RDoC) associated with cognition and is significantly reduced in the brain of schizophrenia patients. To further understand the molecular underpinnings of pathogenesis of schizophrenia, we have performed microarray analyses of the hippocampi from dysbindin knockout mice, and found that genes involved in the lipogenic pathway are suppressed...
April 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/26685100/dysbindin-1-modifies-signaling-and-cellular-localization-of-recombinant-human-d%C3%A2-and-d%C3%A2-receptors
#20
Nathalie Schmieg, Cristina Rocchi, Stefania Romeo, Roberto Maggio, Mark J Millan, Clotilde Mannoury la Cour
Dystrobrevin binding protein-1 (dysbindin-1), a candidate gene for schizophrenia, modulates cognition, synaptic plasticity and frontocortical circuitry and interacts with glutamatergic and dopaminergic transmission. Loss of dysbindin-1 modifies cellular trafficking of dopamine (DA) D2 receptors to increase cell surface expression, but its influence upon signaling has never been characterized. Further, the effects of dysbindin-1 upon closely related D3 receptors remain unexplored. Hence, we examined the impact of dysbindin-1 (isoform A) co-expression on the localization and coupling of human D2L and D3 receptors stably expressed in Chinese hamster ovary or SH-SY5Y cells lacking endogenous dysbindin-1...
March 2016: Journal of Neurochemistry
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