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Mammalian Monoclonal DLG4 Primary Antibody für ISt, IHC - ABIN1304919
Higuchi, Macke, Lee, Miller, Xu, Ikeda, Ikeda: Genetic basis of age-dependent synaptic abnormalities in the retina. in Mammalian genome : official journal of the International Mammalian Genome Society 2015
Show all 336 Pubmed References
Human Monoclonal DLG4 Primary Antibody für BP, ChIP - ABIN4348100
Fogel, Akins, Krupp, Stagi, Stein, Biederer: SynCAMs organize synapses through heterophilic adhesion. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2007
Show all 15 Pubmed References
Human Polyclonal DLG4 Primary Antibody für IP, WB - ABIN1742271
Li, Hu, Höfer, Wong, Cooper, Birnbaum, Hammer, Hofmann: DHHC5 interacts with PDZ domain 3 of post-synaptic density-95 (PSD-95) protein and plays a role in learning and memory. in The Journal of biological chemistry 2010
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Human Polyclonal DLG4 Primary Antibody für IF (p), IHC (p) - ABIN725930
Zhao, Li, Wei, Savage, Zhou, Ma: Ketamine administered to pregnant rats in the second trimester causes long-lasting behavioral disorders in offspring. in Neurobiology of disease 2014
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Mammalian Monoclonal DLG4 Primary Antibody für ISt, IHC - ABIN1304920
Gonzalez-Lozano, Klemmer, Gebuis, Hassan, van Nierop, van Kesteren, Smit, Li: Dynamics of the mouse brain cortical synaptic proteome during postnatal brain development. in Scientific reports 2016
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Cow (Bovine) Polyclonal DLG4 Primary Antibody für WB - ABIN550147
Kim, Sheng: PDZ domain proteins of synapses. in Nature reviews. Neuroscience 2004
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Mouse (Murine) Polyclonal DLG4 Primary Antibody für WB - ABIN152631
Reissner, Boyle, Ye, Carew: Aplysia synapse associated protein (APSAP): identification, characterization, and selective interactions with Shaker-type potassium channels. in Journal of neurochemistry 2008
Human Polyclonal DLG4 Primary Antibody für IHC, IHC (p) - ABIN4348101
Fourie, Kim, Waldvogel, Wong, McGregor, Faull, Montgomery: Differential Changes in Postsynaptic Density Proteins in Postmortem Huntington's Disease and Parkinson's Disease Human Brains. in Journal of neurodegenerative diseases 2015
Human Polyclonal DLG4 Primary Antibody für WB - ABIN6712999
Xie, Wang, Lu, Pan, Chen, Liao: UCH-L1 inhibition involved in CREB dephosphorylation in hippocampal slices. in Journal of molecular neuroscience : MN 2014
Human Monoclonal DLG4 Primary Antibody für IF, IHC - ABIN6675311
Tan, Yao, Hu, Lv, Wan, Zhang, Zhu: Alleviating neuropathic pain mechanical allodynia by increasing Cdh1 in the anterior cingulate cortex. in Molecular pain 2016
findings reveal that Scrib's PDZ1 domain functions in the interaction with Gukh and that the Scrib-Gukh interaction has a key role in epithelial tissue development in Drosophila
The authors find that the tumor suppressor Discs large (Dlg) links the Par complex component atypical Protein Kinase C (aPKC) to the essential spindle orientation factor GukHolder (GukH).
The structure of dlg1 reveals that the core of the dimer is formed by a distinctive six-helix assembly, involving all three conserved helices from each subunit (monomer). The homodimer interface is extended by the C-terminal tail of the L27 domain of Dlg1, which forms a two-stranded antiparallel beta-sheet. The structure reconciles and provides a structural context for a large body of available mutational data.
Strikingly the absence of any of DLG proteins at the presynaptic terminal disrupts the clustering and localization of the calcium channel DmCa1A subunit (Cacophony), decreases the action potential-evoked release probability and alters short-term plasticity.
Exon junction complex (EJC) activity is indispensable for Wg signaling by maintaining an appropriate level of Dsh protein for Wg ligand reception in Drosophila. Genetic and biochemical experiments demonstrate that Dlg1 protein acts independently from its role in cell polarity to protect Dsh protein from lysosomal degradation.
Banderuola (Bnd) is a novel regulator of asymmetric cell division (ACD). The data place Bnd at the top of the hierarchy of the factors involved in ACD, suggesting that its main function is mediating localization and function of Dlg tumor suppressor.
The inactivation of cellular cortex polarization is the most likely target of dlg inactivation in mitosis.
Loss of scrib, dlg and lgl had no effect on gonad formation, but Dlg and Scrib in the gonadal mesoderm acted critically in the somatic wrapping of the pole cells and the internal structure of the Drosophila embryonic gonads.
Gliotactin and Discs large are co-regulated to maintain epithelial integrity.
Hts regulates Dlg targeting to the neuromuscular junction in muscle and the lateral membrane of epithelial cells.
Electron microscopy reveals that during metamorphosis the subsynaptic reticulum vacuolizes in the early stages of synapse dismantling, concomitant with diffuse localization of Dlg.
DlgS97-Metro-DLin-7-type complexes control the proper organization of a synaptic junction; findings accentuate the importance of perisynaptic scaffold complexes for synaptic stabilization and organization
Study provide evidence that scrib and dlg function differentially in anterior and posterior patterning of the follicular epithelium at oogenesis. Further genetic analysis indicates that scrib and dlg act in a common pathway to regulate PFC fate induction.
integrins act through CaMKII activation to control the localization of dlg in the development of NMJ synaptic morphology
conclude that Dlg/Scrib/Lgl are important in regulating cortical polarity, cell size asymmetry and mitotic spindle asymmetry in Drosophila neuroblasts
Isoforms of Dlg are fundamental for neuronal development in Drosophila
role in development of cell boundaries for cell nuclei in Drosophila embryos in conjunction with Strabismus protein
recruitment of DLin-7 to MAGUK-based protein complexes is defined by cell-type specific mechanisms; DLin-7 acts downstream of Sdt in epithelia and downstream of Dlg at synapses
DLG controls glutamate receptor subunit (GluR) composition by selectively stabilizing GluRIIB subunit-containing receptors at the synapse.
Novel spatiotemporal patterns of epithelial tumor invasion in Drosophila disc large egg chambers were studied.
Presenilin-1 targeted morpholino induces cognitive deficits, increased brain Abeta1-42 and decreased synaptic marker PSD-95
The present study aims to show PSD-95 distribution in 3 dimensions.
Study found robust hypersocial behavior in the dyadic interaction test in both PSD95(+/-) males and females. Additionally, male PSD95(+/-) mice exhibited higher levels of aggression and territoriality, while female PSD95(+/-) mice showed increased vocalization upon exposure to an anesthetized female mouse. Both male and female PSD95(+/-) mice revealed mild hypoactivity in the open field but no obvious motor deficit.
PSD95 was essential for Arc assembly into 1.5-MDa complexes and activity-dependent recruitment to excitatory synapses.
Results show the binding of PSD95 to GluN subunit 2A is modulated by CIN.
these data identify PSD95 nanoclusters as a basic structural unit, or building block, of excitatory synapses and their number characterizes synapse size and structural diversity
This study demonstrated that in Chronic social defeat stress leads to changes PSD-95 in hippocampus of young mice.
The authors present evidence that synGAP-alpha1 regulates the composition of the postsynaptic density by restricting binding to the PDZ domains of PSD-95.
In Fmr1 KO neurons, Mdm2 is hyperphosphorylated, nuclear localized basally, and unaffected by MEF2 activation, which our data suggest due to an enhanced interaction with Eukaryotic Elongation Factor 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 KO. Expression of a dephosphomimetic of Mdm2 rescues PSD-95 ubiquitination, degradation and synapse elimination in Fmr1 KO neurons.
tested the effect of five targeted mouse mutations on the assembly of known PSD95 interactors, Kir2.3, Arc, IQsec2/BRAG1 and Adam22
Therefore, our study suggests that CREB and PSD95 are novel substrates of PERK, so inhibition of PERK phosphorylation using GSK2656157 would be beneficial against memory impairment after TBI.
PSD95 and SYP may originate from the different sites, but they are closely related to the formation and maturation of synapse.
Expression levels of brain derived neurotrophic factor, postsynaptic density 95, and p-cyclic-AMP response element binding protein levels were significantly elevated in the testosterone (T) group, but flutamide reduced the T-induced effects in these biomarkers to control levels.
The results suggest that the neurological mechanisms of chronic stress on cognition might be associated with a decrease in hippocampal SYN and PSD95 expression, which is critical for structural synaptic plasticity.
critical roles of PSD-95 in regulating synaptic kainate receptors.
Phenylketonuric mice given a specific nutrient combination showed a significant reduction in PSD-95 expression in the hippocampus, specifically in the granular cell layer of the dentate gyrus, with a similar trend seen in the cornus ammonis 1 (CA1) and cornus ammonis 3 (CA3) pyramidal cell layer.
Lambda-cyhalothrin (LCT) could increase the PSD95 protein level via the ERalpha-dependent Akt pathway, and LCT might disrupt the up-regulation effect of estradiol on PSD95 protein expression via this signaling pathway.
Data indicate a contribution of D2 dopamine receptors to the effects of repetitive transcranial magnetic stimulation (rTMS) on postsynaptic density protein-95 (PSD-95) and cyclin-dependent kinase 5 (CDK5) levels.
Data show that in adult PSD-95 knockout mice, ocular dominance plasticity in visual cortex (V1) was preserved after a stroke lesion in somatosensory cortex (S1).
adult mice lacking interleukin-1 receptor 1 (IL-1R1) exhibit increased expression of both the excitatory scaffolding protein postsynaptic density-95 (PSD-95) and inhibitory scaffolding proteingephyrin, respectively, in the hippocampus.
Data demonstrate a role for SNAP-25 in controlling PSD-95 clustering and open the possibility that genetic reductions of the protein levels may contribute to the pathology through an effect on postsynaptic function and plasticity.
DNA methylation of DLG4 and of human hippocampus and prefrontal cortex in major depression is unchanged in comparison to healthy individuals.
results suggest that rare missense mutations in the candidate PSD genes may increase susceptibility to SZ and/or ASD. These findings may strengthen the theory that rare, non-synonymous variants confer substantial genetic risks for these disorders
in postsynaptic densities, PSD95 palmitoylation, conformation, and its interactions are dynamic when associated with AMPARs and more stable when associated with NMDARs
a dual role for PSD-95 in stabilizing synaptic NMDARs by binding directly to GluN2B but also by promoting synaptic exclusion and degradation of the negative regulator STEP61.
the authors integrate molecular and imaging data from animal models and preterm infants, and find that microglial expression of DLG4 plays a role.
Phosphorylation at Y397 induced a significant increase in affinity for stargazing. The strategy presented here to generate site-specifically phosphorylated PDZ domains provides a detailed understanding of the role of phosphorylation in the regulation of PSD95 interactions.
This study demonstrated that a significant decrease in the protein level of PSD-95 in major depression disorder.
These results indicate that PKC promotes synaptogenesis by activating PSD-95 phosphorylation directly through JNK1 and calcium/calmodulin-dependent kinase II and also by inducing expression of PSD-95 and synaptophysin.
The differences in cortical NMDAR expression and post-synaptic density protein 95 are present in psychiatric disorders and suicide completion and may contribute to different responses to ketamine.
Mutation C>T at the rs13331 in the PSD95 gene is strikingly associated with an increased risk of autism spectrum disorders.
Data indicate the very high affinities of the trimeric ligands to postsynaptic density protein 95 (PSD-95) PDZ domains.
In this review, we focus on palmitoylation of PSD-95, which is a major postsynaptic scaffolding protein and makes discrete postsynaptic nanodomains in a palmitoylation-dependent manner and discuss a determinant role of local palmitoylation cycles
An association was found between reduced PSD95 in the prefrontal cortex and cognitive impairment in patients with either dementia with Lewy bodies or Parkinson's disease dementia.
Docosahexaenoic acid-containing phosphatidylcholines and PSD-95 decrease after loss of synaptophysin and before neuronal loss in patients with Alzheimer's disease.
The postsynaptic membrane protein PSD95 was increased in schizophrenia in CA3 tissue, but not in CA1 tissue.
The crystal structures of the Dlg4 GK domain in complex with two phosphor-Lgl2 peptides reveal the molecular mechanism underlying the specific and phosphorylation-dependent Dlg/Lgl complex formation.
PSD-95 mRNA G-rich region folds into alternate G quadruplex conformations that coexist in equilibrium and miR-125a forms a stable complex with PSD-95 mRNA.
Polymorphisms of DRD1, DLG4 and HOMER1 are associated with opiate abuse.
The PDZ1 domain of PSD-95 has a shallow binding pocket that accommodates a peptide ligand involving far fewer interactions and a micromolar affinity
This gene encodes a member of the membrane-associated guanylate kinase (MAGUK) family. It heteromultimerizes with another MAGUK protein, DLG2, and is recruited into NMDA receptor and potassium channel clusters. These two MAGUK proteins may interact at postsynaptic sites to form a multimeric scaffold for the clustering of receptors, ion channels, and associated signaling proteins. Multiple transcript variants encoding different isoforms have been found for this gene.
, disc large
, discs large
, disk large
, lethal(1)benign wing imaginal disc neoplasm
, lethal(1)discs large
, lethal(2)discs large
, discs, large homolog 4
, postsynaptic density protein 95
, disks large homolog 4
, PSD-95 alpha 2b
, PSD-95 beta
, discs large homolog 4
, synapse-associated protein 90
, synapse-associated protein SAP90
, Tax interaction protein 15
, post-synaptic density protein 95