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  1. Article ; Online: Distinct synaptic pools of DAPK1 differentially regulate activity-dependent synaptic CaMKII accumulation.

    Tullis, Jonathan E / Bayer, K Ulrich

    iScience

    2023  Volume 26, Issue 5, Page(s) 106723

    Abstract: The death-associated protein kinase 1 (DAPK1) regulates the synaptic movement of the ... ...

    Abstract The death-associated protein kinase 1 (DAPK1) regulates the synaptic movement of the Ca
    Language English
    Publishing date 2023-04-23
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.106723
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: CaMKII T286 phosphorylation has distinct essential functions in three forms of long-term plasticity.

    Cook, Sarah G / Rumian, Nicole L / Bayer, K Ulrich

    The Journal of biological chemistry

    2022  Volume 298, Issue 9, Page(s) 102299

    Abstract: ... The ... ...

    Abstract The Ca
    MeSH term(s) Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Hippocampus/metabolism ; Hippocampus/physiology ; Long-Term Synaptic Depression/physiology ; Mice ; N-Methylaspartate/metabolism ; Phosphorylation ; Receptors, Metabotropic Glutamate/genetics ; Receptors, Metabotropic Glutamate/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; Synapses/physiology
    Chemical Substances Receptors, Metabotropic Glutamate ; Receptors, N-Methyl-D-Aspartate ; N-Methylaspartate (6384-92-5) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17)
    Language English
    Publishing date 2022-07-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2022.102299
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
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  3. Article ; Online: Hippocampal-prefrontal theta coupling develops as mice become proficient in associative odorant discrimination learning.

    Ramirez-Gordillo, Daniel / Bayer, K Ulrich / Restrepo, Diego

    eNeuro

    2022  

    Abstract: Learning and memory requires coordinated activity between different regions of the brain. Here we studied the interaction between infralimbic medial prefrontal cortex (mPFC) and hippocampal dorsal CA1 during associative odorant discrimination learning in ...

    Abstract Learning and memory requires coordinated activity between different regions of the brain. Here we studied the interaction between infralimbic medial prefrontal cortex (mPFC) and hippocampal dorsal CA1 during associative odorant discrimination learning in the mouse. We found that as the animal learns to discriminate odorants in a go-no go task, the coupling of high frequency neural oscillations to the phase of theta oscillations (theta-referenced phase-amplitude coupling or tPAC) changes in a manner that results in divergence between rewarded and unrewarded odorant-elicited changes in the theta-phase referenced power (tPRP) for beta and gamma oscillations. In addition, in the proficient animal there was a decrease in the coordinated oscillatory activity between CA1 and mPFC in the presence of the unrewarded odorant. Furthermore, the changes in tPAC resulted in a marked increase in the accuracy for decoding contextual odorant identity from tPRP when the animal became proficient. Finally, we studied the role of Ca
    Language English
    Publishing date 2022-09-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2800598-3
    ISSN 2373-2822 ; 2373-2822
    ISSN (online) 2373-2822
    ISSN 2373-2822
    DOI 10.1523/ENEURO.0259-22.2022
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  4. Article ; Online: Young DAPK1 knockout mice have altered presynaptic function.

    Goodell, Dayton J / Tullis, Jonathan E / Bayer, K Ulrich

    Journal of neurophysiology

    2021  Volume 125, Issue 5, Page(s) 1973–1981

    Abstract: The death-associated protein kinase 1 (DAPK1) has recently been shown to have a physiological function in long-term depression (LTD) of glutamatergic synapses: acute inhibition of DAPK1 blocked the LTD that is normally seen at the hippocampal CA1 synapse ...

    Abstract The death-associated protein kinase 1 (DAPK1) has recently been shown to have a physiological function in long-term depression (LTD) of glutamatergic synapses: acute inhibition of DAPK1 blocked the LTD that is normally seen at the hippocampal CA1 synapse in young mice, and a pharmacogenetic combination approach showed that this specifically required DAPK1-mediated suppression of postsynaptic Ca
    MeSH term(s) Animals ; CA1 Region, Hippocampal/physiology ; Cells, Cultured ; Death-Associated Protein Kinases/physiology ; Electrophysiological Phenomena/physiology ; Glutamic Acid/metabolism ; Long-Term Potentiation/physiology ; Long-Term Synaptic Depression/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
    Chemical Substances Glutamic Acid (3KX376GY7L) ; Dapk1 protein, mouse (EC 2.7.11.1) ; Death-Associated Protein Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2021-04-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80161-6
    ISSN 1522-1598 ; 0022-3077
    ISSN (online) 1522-1598
    ISSN 0022-3077
    DOI 10.1152/jn.00055.2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.224: Show issues Location:
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  5. Article ; Online: CaM Kinase: Still Inspiring at 40.

    Bayer, K Ulrich / Schulman, Howard

    Neuron

    2019  Volume 103, Issue 3, Page(s) 380–394

    Abstract: ... The ... ...

    Abstract The Ca
    MeSH term(s) Amino Acid Sequence ; Animals ; Brain/enzymology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/chemistry ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/physiology ; Cognition/physiology ; Humans ; Long-Term Potentiation/physiology ; Memory/physiology ; Models, Molecular ; Multigene Family ; Nerve Tissue Proteins/chemistry ; Nerve Tissue Proteins/physiology ; Phosphorylation ; Protein Conformation ; Protein Domains ; Protein Interaction Mapping ; Protein Processing, Post-Translational ; Protein-Serine-Threonine Kinases/classification ; Protein-Serine-Threonine Kinases/physiology ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synaptic Transmission
    Chemical Substances NR2B NMDA receptor ; Nerve Tissue Proteins ; Receptors, N-Methyl-D-Aspartate ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17)
    Language English
    Publishing date 2019-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2019.05.033
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2496: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 92: Show issues

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  6. Article ; Online: Stimulating β-adrenergic receptors promotes synaptic potentiation by switching CaMKII movement from LTD to LTP mode.

    Larsen, Matthew E / Buonarati, Olivia R / Qian, Hai / Hell, Johannes W / Bayer, K Ulrich

    The Journal of biological chemistry

    2023  Volume 299, Issue 6, Page(s) 104706

    Abstract: Learning, memory, and cognition are thought to require synaptic plasticity, specifically including hippocampal long-term potentiation and depression (LTP and LTD). LTP versus LTD is induced by high-frequency stimulation versus low-frequency, but ... ...

    Abstract Learning, memory, and cognition are thought to require synaptic plasticity, specifically including hippocampal long-term potentiation and depression (LTP and LTD). LTP versus LTD is induced by high-frequency stimulation versus low-frequency, but stimulating β-adrenergic receptors (βARs) enables LTP induction also by low-frequency stimulation (1 Hz) or theta frequencies (∼5 Hz) that do not cause plasticity by themselves. In contrast to high-frequency stimulation-LTP, such βAR-LTP requires Ca
    MeSH term(s) Long-Term Potentiation ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Receptors, Adrenergic, beta/metabolism ; D-Aspartic Acid/metabolism ; D-Aspartic Acid/pharmacology ; Long-Term Synaptic Depression/physiology ; Hippocampus/metabolism ; Synapses/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism
    Chemical Substances Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Receptors, Adrenergic, beta ; D-Aspartic Acid (4SR0Q8YD1X) ; Receptors, N-Methyl-D-Aspartate
    Language English
    Publishing date 2023-04-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.104706
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
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  7. Article ; Online: Decreased nitrosylation of CaMKII causes aging-associated impairments in memory and synaptic plasticity in mice.

    Rumian, Nicole L / Freund, Ronald K / Dell'Acqua, Mark L / Coultrap, Steven J / Bayer, K Ulrich

    Science signaling

    2023  Volume 16, Issue 795, Page(s) eade5892

    Abstract: CaMKII has molecular memory functions because transient calcium ion stimuli can induce long-lasting increases in its synaptic localization and calcium ion-independent (autonomous) activity, thereby leaving memory traces of calcium ion stimuli beyond ... ...

    Abstract CaMKII has molecular memory functions because transient calcium ion stimuli can induce long-lasting increases in its synaptic localization and calcium ion-independent (autonomous) activity, thereby leaving memory traces of calcium ion stimuli beyond their duration. The synaptic effects of two mechanisms that induce CaMKII autonomy are well studied: autophosphorylation at threonine-286 and binding to GluN2B. Here, we examined the neuronal functions of additional autonomy mechanisms: nitrosylation and oxidation of the CaMKII regulatory domain. We generated a knock-in mouse line with mutations that render the CaMKII regulatory domain nitrosylation/oxidation-incompetent, CaMKII
    MeSH term(s) Animals ; Mice ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Hippocampus/metabolism ; Long-Term Potentiation/physiology ; Neuronal Plasticity ; Phosphorylation ; Synapses/metabolism
    Chemical Substances Calcium (SY7Q814VUP) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Camk2a protein, mouse (EC 2.7.11.17)
    Language English
    Publishing date 2023-07-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.ade5892
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  8. Article ; Online: CaMKII holoenzyme mechanisms that govern the LTP versus LTD decision.

    Cook, Sarah G / Buonarati, Olivia R / Coultrap, Steven J / Bayer, K Ulrich

    Science advances

    2021  Volume 7, Issue 16

    Abstract: Higher brain functions are thought to require synaptic frequency decoding that can lead to long-term potentiation (LTP) or depression (LTD). We show that the LTP versus LTD decision is determined by complex cross-regulation of T286 and T305/306 ... ...

    Abstract Higher brain functions are thought to require synaptic frequency decoding that can lead to long-term potentiation (LTP) or depression (LTD). We show that the LTP versus LTD decision is determined by complex cross-regulation of T286 and T305/306 autophosphorylation within the 12meric CaMKII holoenzyme, which enabled molecular computation of stimulus frequency, amplitude, and duration. Both LTP and LTD require T286 phosphorylation, but T305/306 phosphorylation selectively promoted LTD. In response to excitatory LTP versus LTD stimuli, the differential T305/306 phosphorylation directed CaMKII movement to either excitatory or inhibitory synapses, thereby coordinating plasticity at both synapse types. Fast T305/306 phosphorylation required prior T286 phosphorylation and then curbed CaMKII activity by two mechanisms: (i) a cis-subunit reaction reduced both Ca
    Language English
    Publishing date 2021-04-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abe2300
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  9. Article ; Online: Aβ-induced synaptic impairments require CaMKII activity that is stimulated by indirect signaling events.

    Brown, Carolyn Nicole / Rumian, Nicole L / Tullis, Jonathan E / Coultrap, Steven J / Bayer, K Ulrich

    iScience

    2022  Volume 25, Issue 6, Page(s) 104368

    Abstract: Aβ bears homology to the CaMKII regulatory domain, and peptides derived from this domain can bind and disrupt the CaMKII holoenzyme, suggesting that Aβ could have a similar effect. Notably, Aβ impairs the synaptic CaMKII accumulation that is mediated by ... ...

    Abstract Aβ bears homology to the CaMKII regulatory domain, and peptides derived from this domain can bind and disrupt the CaMKII holoenzyme, suggesting that Aβ could have a similar effect. Notably, Aβ impairs the synaptic CaMKII accumulation that is mediated by GluN2B binding, which requires CaMKII assembly into holoenzymes. Furthermore, this Aβ-induced impairment is prevented by CaMKII inhibitors that should also inhibit the putative direct Aβ binding. However, our study did not find any evidence for direct effects of Aβ on CaMKII: Aβ did not directly disrupt CaMKII holoenzymes, GluN2B binding, T286 autophosphorylation, or kinase activity
    Language English
    Publishing date 2022-05-06
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2022.104368
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  10. Article ; Online: The CaMKII K42M and K42R mutations are equivalent in suppressing kinase activity and targeting.

    Tullis, Jonathan E / Rumian, Nicole L / Brown, Carolyn Nicole / Bayer, K Ulrich

    PloS one

    2020  Volume 15, Issue 7, Page(s) e0236478

    Abstract: CaMKII is an important mediator of forms of synaptic plasticity that are thought to underly learning and memory. The CaMKII mutants K42M and K42R have been used interchangeably as research tools, although some reported phenotypic differences suggest that ...

    Abstract CaMKII is an important mediator of forms of synaptic plasticity that are thought to underly learning and memory. The CaMKII mutants K42M and K42R have been used interchangeably as research tools, although some reported phenotypic differences suggest that they may differ in the extent to which they impair ATP binding. Here, we directly compared the two mutations at the high ATP concentrations that exist within cells (~4 mM). We found that both mutations equally blocked GluA1 phosphorylation in vitro and GluN2B binding within cells. Both mutations also reduced but did not completely abolish CaMKII T286 autophosphorylation in vitro or CaMKII movement to excitatory synapses in neurons. Thus, despite previously suggested differences, both mutations appear to interfere with ATP binding to the same extent.
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/chemistry ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics ; Cells, Cultured ; Female ; Glutamic Acid/pharmacology ; HEK293 Cells ; Hippocampus/cytology ; Humans ; Male ; Movement ; Mutation/genetics ; Phosphorylation ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism
    Chemical Substances NR2B NMDA receptor ; Receptors, N-Methyl-D-Aspartate ; Glutamic Acid (3KX376GY7L) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-07-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0236478
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