Academic literature on the topic 'PSD-93'

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Journal articles on the topic "PSD-93"

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Tao, Feng, John Skinner, Ya Yang, and Roger A. Johns. "Effect of PSD-95/SAP90 and/or PSD-93/Chapsyn-110 Deficiency on the Minimum Alveolar Anesthetic Concentration of Halothane in Mice." Anesthesiology 112, no. 6 (2010): 1444–51. http://dx.doi.org/10.1097/aln.0b013e3181dcd3dc.

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Background The authors have previously shown that the clinically relevant concentrations of inhalational anesthetics dose-dependently inhibit the postsynaptic density protein (PSD)-95, Dlg, and ZO-1 domain-mediated protein interactions between N-methyl-d-aspartate receptors and PSD-95/synaptic-associated protein (SAP) 90 or PSD-93/Chapsyn-110 and that the knockdown of spinal PSD-95/SAP90 significantly reduces the minimum alveolar concentration (MAC) for isoflurane in rats. Methods The authors designed antisense oligodeoxynucleotides based on the mouse PSD-95/SAP90 and PSD-93/Chapsyn-110 messenger RNAs that correspond to their PSD-95, Dlg, and ZO-1 domain nucleotides and can specifically knock down the respective proteins. The authors intrathecally injected antisense oligodeoxynucleotides into wild-type and PSD-93/Chapsyn-110 knockout mice to investigate the effect of PSD-95/SAP90 and/or PSD-93/Chapsyn-110 deficiency on halothane anesthesia. Results Both PSD-95/SAP90 and PSD-93/Chapsyn-110 antisense oligodeoxynucleotides caused a dose-dependent and significant reduction in the MAC of halothane in wild-type mice. The intrathecal injection of PSD-95/SAP90 antisense oligodeoxynucleotide at different doses (25 and 50 microg) reduced halothane MAC by 40 and 55%, respectively, and intrathecal injection of PSD-93/Chapsyn-110 antisense oligodeoxynucleotide at different doses (12 and 24 microg) reduced halothane MAC by 25 and 53%, respectively. The PSD-95/SAP90 antisense oligodeoxynucleotide showed similar effect on halothane MAC in wild-type and PSD-93/Chapsyn-110 knockout mice, suggesting that the combination of PSD-95/SAP90 knockdown with PSD-93/Chapsyn-110 deletion did not have an additive effect on halothane anesthesia. Conclusions The current results indicate that PSD-95/SAP90 and PSD-93/Chapsyn-110 are involved in the molecular mechanisms of halothane anesthesia and that the functional role of PSD-95/SAP90 in halothane anesthesia is not enhanced after PSD-93/Chapsyn-110 deletion.
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Girard, Beatrice M., Laura A. Merriam, John D. Tompkins, Margaret A. Vizzard, and Rodney L. Parsons. "Decrease in neuronal nicotinic acetylcholine receptor subunit and PSD-93 transcript levels in the male mouse MPG after cavernous nerve injury or explant culture." American Journal of Physiology-Renal Physiology 305, no. 10 (2013): F1504—F1512. http://dx.doi.org/10.1152/ajprenal.00343.2013.

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Quantitative real-time PCR was used to test whether cavernous nerve injury leads to a decrease in major pelvic ganglia (MPG) neuronal nicotinic ACh receptor (nAChR) subunit and postsynaptic density (PSD)-93 transcript levels. Subunits α3, β4, and α7, commonly expressed in the MPG, were selected for analysis. After 72 h in explant culture, MPG transcript levels for α3, β4, α7, and PSD-93 were significantly depressed. Three days after cavernous nerve axotomy or crush in vivo, transcript levels for α3, β4, and PSD-93, but not for α7, were significantly depressed. Three days after dissection of the cavernous nerve free of underlying tissue and application of a 5-mm lateral stretch (manipulation), transcript levels for α3and PSD-93 were also significantly decreased. Seven days after all three surgical procedures, α3transcript levels remained depressed, but PSD-93 transcript levels were still decreased only after axotomy or nerve crush. At 30 days postsurgery, transcript levels for the nAChR subunits and PSD-93 had recovered. ACh-induced currents were significantly smaller in MPG neurons dissociated from 3-day explant cultured ganglia than from those recorded in neurons dissociated from acutely isolated ganglia; this observation provides direct evidence showing that a decrease in nAChR function was coincident with a decrease in nAChR subunit transcript levels. We conclude that a downregulation of nAChR subunit and PSD-93 expression after cavernous nerve injury, or even manipulation, could interrupt synaptic transmission within the MPG and thus contribute to the loss of neural control of urogenital organs after pelvic surgeries.
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DeGiorgis, Joseph A., James A. Galbraith, Ayse Dosemeci, Xiaobing Chen, and Thomas S. Reese. "Distribution of the scaffolding proteins PSD-95, PSD-93, and SAP97 in isolated PSDs." Brain Cell Biology 35, no. 4-6 (2006): 239–50. http://dx.doi.org/10.1007/s11068-007-9017-0.

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Löwel, Siegrid. "Yin und Yang beim Lernen im jungen Gehirn: Balance von PSD-95 und PSD-93." BIOspektrum 26, no. 2 (2020): 140–42. http://dx.doi.org/10.1007/s12268-020-1355-9.

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Tao, Yuan-Xiang, Frederick Kauer, David S. Bredt, and Roger A. Johns. "Reduction of Neuropathic Pain in Mice Lacking PSD-93." Anesthesiology 96, Sup 2 (2002): A829. http://dx.doi.org/10.1097/00000542-200209002-00829.

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Sun, Q., and G. G. Turrigiano. "PSD-95 and PSD-93 Play Critical But Distinct Roles in Synaptic Scaling Up and Down." Journal of Neuroscience 31, no. 18 (2011): 6800–6808. http://dx.doi.org/10.1523/jneurosci.5616-10.2011.

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Fiorentini, Monica, Ann Kallehauge Nielsen, Ole Kristensen, Jette S. Kastrup, and Michael Gajhede. "Structure of the first PDZ domain of human PSD-93." Acta Crystallographica Section F Structural Biology and Crystallization Communications 65, no. 12 (2009): 1254–57. http://dx.doi.org/10.1107/s1744309109043267.

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Carlisle, Holly J., Ann E. Fink, Seth G. N. Grant, and Thomas J. O’Dell. "Opposing effects of PSD-93 and PSD-95 on long-term potentiation and spike timing-dependent plasticity." Journal of Physiology 586, no. 24 (2008): 5885–900. http://dx.doi.org/10.1113/jphysiol.2008.163469.

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Guo, Ming-Lei, Bing Xue, Dao-Zhong Jin, Li-Min Mao, and John Q. Wang. "Interactions and phosphorylation of postsynaptic density 93 (PSD-93) by extracellular signal-regulated kinase (ERK)." Brain Research 1465 (July 2012): 18–25. http://dx.doi.org/10.1016/j.brainres.2012.05.026.

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LARSSON, Mårten, Göran HJÄLM, Amos M. SAKWE, et al. "Selective interaction of megalin with postsynaptic density-95 (PSD-95)-like membrane-associated guanylate kinase (MAGUK) proteins." Biochemical Journal 373, no. 2 (2003): 381–91. http://dx.doi.org/10.1042/bj20021958.

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Megalin is an integral membrane receptor belonging to the low-density lipoprotein receptor family. In addition to its role as an endocytotic receptor, megalin has also been proposed to have signalling functions. Using interaction cloning in yeast, we identified the membrane-associated guanylate kinase family member postsynaptic density-95 (PSD-95) as an interaction partner for megalin. PSD-95 and a truncated version of megalin were co-immunoprecipitated from HEK-293 cell lysates overexpressing the two proteins, which confirmed the interaction. The two proteins were found to be co-localized in these cells by confocal microscopy. Immunocytochemical studies showed that cells in the parathyroid, proximal tubuli of the kidney and placenta express both megalin and PSD-95. We found that the interaction between the two proteins is mediated by the binding of the C-terminus of megalin, which has a type I PSD-95/Drosophila discs-large/zona occludens 1 (PDZ)-binding motif, to the PDZ2 domain of PSD-95. The PSD-95-like membrane-associated guanylate kinase (‘MAGUK’) family contains three additional members: PSD-93, synapse-associated protein 97 (SAP97) and SAP102. We detected these proteins, apart from SAP102, in parathyroid chief cells, a cell type having a marked expression of megalin. The PDZ2 domains of PSD-93 and SAP102 were also shown to interact with megalin, whereas no interaction was detected for SAP97. The SAP97 PDZ2 domain differed at four positions from the other members of the PSD-95 subfamily. One of these residues was Thr389, located in the αB-helix and part of the hydrophobic pocket of the PDZ2 domain. Surface plasmon resonance experiments revealed that mutation of SAP97 Thr389 to alanine, as with the other PSD-95-like membrane-associated guanylate kinases, induced binding to megalin.
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Dissertations / Theses on the topic "PSD-93"

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Stodieck, Sophia Katharina [Verfasser], Siegrid [Akademischer Betreuer] [Gutachter] Loewel, Tim [Gutachter] Gollisch, and Oliver M. [Gutachter] Schlueter. "The role of postsynaptic density (PSD) proteins PSD-95 and PSD-93 for mouse visual cortical plasticity and vision / Sophia Katharina Stodieck ; Gutachter: Siegrid Loewel, Tim Gollisch, Oliver M. Schlueter ; Betreuer: Siegrid Loewel." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1140641999/34.

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Krüger, Juliane Marie [Verfasser], Oliver [Akademischer Betreuer] Schlüter, and Nils [Akademischer Betreuer] Brose. "Expression and function of PSD-93 isoforms in hippocampal synapses / Juliane Marie Krüger. Gutachter: Nils Brose. Betreuer: Oliver Schlüter." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2010. http://d-nb.info/1042639019/34.

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Favaro, Plinio Das Neves [Verfasser], Oliver [Akademischer Betreuer] Schlüter, Walter [Akademischer Betreuer] Stühmer, Holger [Akademischer Betreuer] Taschenberger, Siegrid [Akademischer Betreuer] Löwel, and Michael [Akademischer Betreuer] Hörner. "Roles of PSD-93 and environmental enrichment in cortical synapses / Plinio Das Neves Favaro. Betreuer: Oliver Schlüter. Gutachter: Walter Stühmer ; Holger Taschenberger ; Siegrid Löwel ; Michael Hörner." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1078774250/34.

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Stodieck, Sophia Katharina. "The role of postsynaptic density (PSD) proteins PSD-95 and PSD-93 for mouse visual cortical plasticity and vision." Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-0023-3F15-A.

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Krüger, Juliane Marie. "Expression and function of PSD-93 isoforms in hippocampal synapses." Doctoral thesis, 2010. http://hdl.handle.net/11858/00-1735-0000-0006-ADB6-3.

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Das, Neves Favaro Plinio. "Roles of PSD-93 and environmental enrichment in cortical synapses." Doctoral thesis, 2014. http://hdl.handle.net/11858/00-1735-0000-0023-9681-1.

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Duda, Joana-Kristin. "The role of DLG-MAGUKs in mediating signaling specificity at the postsynaptic density." Doctoral thesis, 2018. http://hdl.handle.net/11858/00-1735-0000-002E-E570-E.

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