PSA-NCAM : synaptic functions mediated by its interactions with proteoglycans and glutamate receptors
Dynamic regulation of glycosylation of the neural cell adhesion molecule (NCAM) by an unusual large negatively charged polysialic acid (PSA) is the major prerequisite for correct formation of brain circuitries during development and for normal synaptic plasticity, learning and memory in the adult. T...
Ausführliche Beschreibung
Autor*in: |
Senkov, Oleg [verfasserIn] Tikhobrazova, Olga [verfasserIn] Dityatev, Alexander [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
25 January 2012 |
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Schlagwörter: |
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Anmerkung: |
Available online 25 January 2012 Gesehen am 06.07.2018 |
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Umfang: |
5 |
Übergeordnetes Werk: |
Enthalten in: International journal of biochemistry & cell biology - Amsterdam : Elsevier, 1995, 44(2012), 4, Seite 591-595 |
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Übergeordnetes Werk: |
volume:44 ; year:2012 ; number:4 ; pages:591-595 ; extent:5 |
Links: |
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DOI / URN: |
10.1016/j.biocel.2012.01.008 |
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Katalog-ID: |
1577385683 |
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520 | |a Dynamic regulation of glycosylation of the neural cell adhesion molecule (NCAM) by an unusual large negatively charged polysialic acid (PSA) is the major prerequisite for correct formation of brain circuitries during development and for normal synaptic plasticity, learning and memory in the adult. Traditionally, PSA is viewed as a de-adhesive highly hydrated molecule, which interferes with cell adhesion and promotes cellular/synaptic dynamics by steric hindrance. Analysis of synaptic functions of PSA-NCAM highlighted additional features of this molecule. First, PSA promotes interaction of NCAM with heparan sulfate proteoglycans and thus stimulates synaptogenesis. Second, PSA-NCAM modulates glutamate receptors: it restrains activity of extrasynaptic GluN2B-containing NMDA receptors and facilitates activity of a subset of AMPA receptors. Perturbation in polysialylation and/or NCAM expression in mouse models recapitulates many symptoms of human brain disorders such as schizophrenia, depression, anxiety and Alzheimer's disease. | ||
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2012 |
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10.1016/j.biocel.2012.01.008 doi (DE-627)1577385683 (DE-576)507385683 (DE-599)BSZ507385683 (OCoLC)1341013496 DE-627 ger DE-627 rda eng Senkov, Oleg verfasserin (DE-588)132778882 (DE-627)526932082 (DE-576)299407454 aut PSA-NCAM synaptic functions mediated by its interactions with proteoglycans and glutamate receptors Oleg Senkov, Olga Tikhobrazova, Alexander Dityatev 25 January 2012 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Available online 25 January 2012 Gesehen am 06.07.2018 Dynamic regulation of glycosylation of the neural cell adhesion molecule (NCAM) by an unusual large negatively charged polysialic acid (PSA) is the major prerequisite for correct formation of brain circuitries during development and for normal synaptic plasticity, learning and memory in the adult. Traditionally, PSA is viewed as a de-adhesive highly hydrated molecule, which interferes with cell adhesion and promotes cellular/synaptic dynamics by steric hindrance. Analysis of synaptic functions of PSA-NCAM highlighted additional features of this molecule. First, PSA promotes interaction of NCAM with heparan sulfate proteoglycans and thus stimulates synaptogenesis. Second, PSA-NCAM modulates glutamate receptors: it restrains activity of extrasynaptic GluN2B-containing NMDA receptors and facilitates activity of a subset of AMPA receptors. Perturbation in polysialylation and/or NCAM expression in mouse models recapitulates many symptoms of human brain disorders such as schizophrenia, depression, anxiety and Alzheimer's disease. GluN2B Learning NCAM Polysialic acid PSA PSA-NCAM Synaptic plasticity Tikhobrazova, Olga verfasserin (DE-588)1162363231 (DE-627)1026032369 (DE-576)507385594 aut Dityatev, Alexander verfasserin (DE-588)1027216242 (DE-627)728611465 (DE-576)37262393X aut Enthalten in International journal of biochemistry & cell biology Amsterdam : Elsevier, 1995 44(2012), 4, Seite 591-595 Online-Ressource (DE-627)320412261 (DE-600)2001470-3 (DE-576)094531323 1878-5875 nnns volume:44 year:2012 number:4 pages:591-595 extent:5 http://dx.doi.org/10.1016/j.biocel.2012.01.008 Verlag Resolving-System Volltext http://www.sciencedirect.com/science/article/pii/S135727251200012X Verlag Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 AR 44 2012 4 591-595 5 2013 01 DE-16-250 3016623323 00 --%%-- --%%-- --%%-- --%%-- l01 06-07-18 2013 01 DE-16-250 00 s hd2012 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_3 2013 01 DE-16-250 03 s s_5 2013 01 DE-16-250 04 p (DE-627)1500210943 Senkov, Oleg 2013 01 DE-16-250 04 k (DE-627)1416741267 Neurologische Universitätsklinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 |
spelling |
10.1016/j.biocel.2012.01.008 doi (DE-627)1577385683 (DE-576)507385683 (DE-599)BSZ507385683 (OCoLC)1341013496 DE-627 ger DE-627 rda eng Senkov, Oleg verfasserin (DE-588)132778882 (DE-627)526932082 (DE-576)299407454 aut PSA-NCAM synaptic functions mediated by its interactions with proteoglycans and glutamate receptors Oleg Senkov, Olga Tikhobrazova, Alexander Dityatev 25 January 2012 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Available online 25 January 2012 Gesehen am 06.07.2018 Dynamic regulation of glycosylation of the neural cell adhesion molecule (NCAM) by an unusual large negatively charged polysialic acid (PSA) is the major prerequisite for correct formation of brain circuitries during development and for normal synaptic plasticity, learning and memory in the adult. Traditionally, PSA is viewed as a de-adhesive highly hydrated molecule, which interferes with cell adhesion and promotes cellular/synaptic dynamics by steric hindrance. Analysis of synaptic functions of PSA-NCAM highlighted additional features of this molecule. First, PSA promotes interaction of NCAM with heparan sulfate proteoglycans and thus stimulates synaptogenesis. Second, PSA-NCAM modulates glutamate receptors: it restrains activity of extrasynaptic GluN2B-containing NMDA receptors and facilitates activity of a subset of AMPA receptors. Perturbation in polysialylation and/or NCAM expression in mouse models recapitulates many symptoms of human brain disorders such as schizophrenia, depression, anxiety and Alzheimer's disease. GluN2B Learning NCAM Polysialic acid PSA PSA-NCAM Synaptic plasticity Tikhobrazova, Olga verfasserin (DE-588)1162363231 (DE-627)1026032369 (DE-576)507385594 aut Dityatev, Alexander verfasserin (DE-588)1027216242 (DE-627)728611465 (DE-576)37262393X aut Enthalten in International journal of biochemistry & cell biology Amsterdam : Elsevier, 1995 44(2012), 4, Seite 591-595 Online-Ressource (DE-627)320412261 (DE-600)2001470-3 (DE-576)094531323 1878-5875 nnns volume:44 year:2012 number:4 pages:591-595 extent:5 http://dx.doi.org/10.1016/j.biocel.2012.01.008 Verlag Resolving-System Volltext http://www.sciencedirect.com/science/article/pii/S135727251200012X Verlag Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 AR 44 2012 4 591-595 5 2013 01 DE-16-250 3016623323 00 --%%-- --%%-- --%%-- --%%-- l01 06-07-18 2013 01 DE-16-250 00 s hd2012 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_3 2013 01 DE-16-250 03 s s_5 2013 01 DE-16-250 04 p (DE-627)1500210943 Senkov, Oleg 2013 01 DE-16-250 04 k (DE-627)1416741267 Neurologische Universitätsklinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 |
allfields_unstemmed |
10.1016/j.biocel.2012.01.008 doi (DE-627)1577385683 (DE-576)507385683 (DE-599)BSZ507385683 (OCoLC)1341013496 DE-627 ger DE-627 rda eng Senkov, Oleg verfasserin (DE-588)132778882 (DE-627)526932082 (DE-576)299407454 aut PSA-NCAM synaptic functions mediated by its interactions with proteoglycans and glutamate receptors Oleg Senkov, Olga Tikhobrazova, Alexander Dityatev 25 January 2012 5 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Available online 25 January 2012 Gesehen am 06.07.2018 Dynamic regulation of glycosylation of the neural cell adhesion molecule (NCAM) by an unusual large negatively charged polysialic acid (PSA) is the major prerequisite for correct formation of brain circuitries during development and for normal synaptic plasticity, learning and memory in the adult. Traditionally, PSA is viewed as a de-adhesive highly hydrated molecule, which interferes with cell adhesion and promotes cellular/synaptic dynamics by steric hindrance. Analysis of synaptic functions of PSA-NCAM highlighted additional features of this molecule. First, PSA promotes interaction of NCAM with heparan sulfate proteoglycans and thus stimulates synaptogenesis. Second, PSA-NCAM modulates glutamate receptors: it restrains activity of extrasynaptic GluN2B-containing NMDA receptors and facilitates activity of a subset of AMPA receptors. Perturbation in polysialylation and/or NCAM expression in mouse models recapitulates many symptoms of human brain disorders such as schizophrenia, depression, anxiety and Alzheimer's disease. GluN2B Learning NCAM Polysialic acid PSA PSA-NCAM Synaptic plasticity Tikhobrazova, Olga verfasserin (DE-588)1162363231 (DE-627)1026032369 (DE-576)507385594 aut Dityatev, Alexander verfasserin (DE-588)1027216242 (DE-627)728611465 (DE-576)37262393X aut Enthalten in International journal of biochemistry & cell biology Amsterdam : Elsevier, 1995 44(2012), 4, Seite 591-595 Online-Ressource (DE-627)320412261 (DE-600)2001470-3 (DE-576)094531323 1878-5875 nnns volume:44 year:2012 number:4 pages:591-595 extent:5 http://dx.doi.org/10.1016/j.biocel.2012.01.008 Verlag Resolving-System Volltext http://www.sciencedirect.com/science/article/pii/S135727251200012X Verlag Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 AR 44 2012 4 591-595 5 2013 01 DE-16-250 3016623323 00 --%%-- --%%-- --%%-- --%%-- l01 06-07-18 2013 01 DE-16-250 00 s hd2012 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_3 2013 01 DE-16-250 03 s s_5 2013 01 DE-16-250 04 p (DE-627)1500210943 Senkov, Oleg 2013 01 DE-16-250 04 k (DE-627)1416741267 Neurologische Universitätsklinik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_1 |
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PSA-NCAM synaptic functions mediated by its interactions with proteoglycans and glutamate receptors Oleg Senkov, Olga Tikhobrazova, Alexander Dityatev |
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PSA-NCAM synaptic functions mediated by its interactions with proteoglycans and glutamate receptors |
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Dynamic regulation of glycosylation of the neural cell adhesion molecule (NCAM) by an unusual large negatively charged polysialic acid (PSA) is the major prerequisite for correct formation of brain circuitries during development and for normal synaptic plasticity, learning and memory in the adult. Traditionally, PSA is viewed as a de-adhesive highly hydrated molecule, which interferes with cell adhesion and promotes cellular/synaptic dynamics by steric hindrance. Analysis of synaptic functions of PSA-NCAM highlighted additional features of this molecule. First, PSA promotes interaction of NCAM with heparan sulfate proteoglycans and thus stimulates synaptogenesis. Second, PSA-NCAM modulates glutamate receptors: it restrains activity of extrasynaptic GluN2B-containing NMDA receptors and facilitates activity of a subset of AMPA receptors. Perturbation in polysialylation and/or NCAM expression in mouse models recapitulates many symptoms of human brain disorders such as schizophrenia, depression, anxiety and Alzheimer's disease. Available online 25 January 2012 Gesehen am 06.07.2018 |
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Dynamic regulation of glycosylation of the neural cell adhesion molecule (NCAM) by an unusual large negatively charged polysialic acid (PSA) is the major prerequisite for correct formation of brain circuitries during development and for normal synaptic plasticity, learning and memory in the adult. Traditionally, PSA is viewed as a de-adhesive highly hydrated molecule, which interferes with cell adhesion and promotes cellular/synaptic dynamics by steric hindrance. Analysis of synaptic functions of PSA-NCAM highlighted additional features of this molecule. First, PSA promotes interaction of NCAM with heparan sulfate proteoglycans and thus stimulates synaptogenesis. Second, PSA-NCAM modulates glutamate receptors: it restrains activity of extrasynaptic GluN2B-containing NMDA receptors and facilitates activity of a subset of AMPA receptors. Perturbation in polysialylation and/or NCAM expression in mouse models recapitulates many symptoms of human brain disorders such as schizophrenia, depression, anxiety and Alzheimer's disease. Available online 25 January 2012 Gesehen am 06.07.2018 |
abstract_unstemmed |
Dynamic regulation of glycosylation of the neural cell adhesion molecule (NCAM) by an unusual large negatively charged polysialic acid (PSA) is the major prerequisite for correct formation of brain circuitries during development and for normal synaptic plasticity, learning and memory in the adult. Traditionally, PSA is viewed as a de-adhesive highly hydrated molecule, which interferes with cell adhesion and promotes cellular/synaptic dynamics by steric hindrance. Analysis of synaptic functions of PSA-NCAM highlighted additional features of this molecule. First, PSA promotes interaction of NCAM with heparan sulfate proteoglycans and thus stimulates synaptogenesis. Second, PSA-NCAM modulates glutamate receptors: it restrains activity of extrasynaptic GluN2B-containing NMDA receptors and facilitates activity of a subset of AMPA receptors. Perturbation in polysialylation and/or NCAM expression in mouse models recapitulates many symptoms of human brain disorders such as schizophrenia, depression, anxiety and Alzheimer's disease. Available online 25 January 2012 Gesehen am 06.07.2018 |
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