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  1. Article: The Disruption of NMDAR/TRPM4 Death Signaling with TwinF Interface Inhibitors: A New Pharmacological Principle for Neuroprotection.

    Yan, Jing / Bading, Hilmar

    Pharmaceuticals (Basel, Switzerland)

    2023  Volume 16, Issue 8

    Abstract: With the discovery that the acquisition of toxic features by extrasynaptic NMDA receptors (NMDARs) involves their physical interaction with the non-selective cation channel, TRPM4, it has become possible to develop a new pharmacological principle for ... ...

    Abstract With the discovery that the acquisition of toxic features by extrasynaptic NMDA receptors (NMDARs) involves their physical interaction with the non-selective cation channel, TRPM4, it has become possible to develop a new pharmacological principle for neuroprotection, namely the disruption of the NMDAR/TRPM4 death signaling complex. This can be accomplished through the expression of the TwinF domain, a 57-amino-acid-long stretch of TRPM4 that mediates its interaction with NMDARs, but also using small molecule TwinF interface (TI) inhibitors, also known as NMDAR/TRPM4 interaction interface inhibitors. Both TwinF and small molecule TI inhibitors detoxify extrasynaptic NMDARs without interfering with synaptic NMDARs, which serve important physiological functions in the brain. As the toxic signaling of extrasynaptic NMDARs contributes to a wide range of neurodegenerative conditions, TI inhibitors may offer therapeutic options for currently untreatable human neurodegenerative diseases including Amyotrophic Lateral Sclerosis, Alzheimer's disease, and Huntington's disease.
    Language English
    Publishing date 2023-07-31
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph16081085
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: TwinF interface inhibitor FP802 stops loss of motor neurons and mitigates disease progression in a mouse model of ALS.

    Yan, Jing / Wang, Yu Meng / Hellwig, Andrea / Bading, Hilmar

    Cell reports. Medicine

    2024  Volume 5, Issue 2, Page(s) 101413

    Abstract: Toxic signaling by extrasynaptic NMDA receptors (eNMDARs) is considered an important promoter of amyotrophic lateral sclerosis (ALS) disease progression. To exploit this therapeutically, we take advantage of TwinF interface (TI) inhibition, a ... ...

    Abstract Toxic signaling by extrasynaptic NMDA receptors (eNMDARs) is considered an important promoter of amyotrophic lateral sclerosis (ALS) disease progression. To exploit this therapeutically, we take advantage of TwinF interface (TI) inhibition, a pharmacological principle that, contrary to classical NMDAR pharmacology, allows selective elimination of eNMDAR-mediated toxicity via disruption of the NMDAR/TRPM4 death signaling complex while sparing the vital physiological functions of synaptic NMDARs. Post-disease onset treatment of the SOD1
    MeSH term(s) Mice ; Animals ; Humans ; Amyotrophic Lateral Sclerosis/drug therapy ; Amyotrophic Lateral Sclerosis/pathology ; Superoxide Dismutase/metabolism ; Superoxide Dismutase/pharmacology ; Superoxide Dismutase/therapeutic use ; Mice, Transgenic ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Disease Models, Animal ; Disease Progression ; TRPM Cation Channels
    Chemical Substances Superoxide Dismutase (EC 1.15.1.1) ; TRPM4 protein, mouse ; TRPM Cation Channels
    Language English
    Publishing date 2024-02-06
    Publishing country United States
    Document type Journal Article
    ISSN 2666-3791
    ISSN (online) 2666-3791
    DOI 10.1016/j.xcrm.2024.101413
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  3. Article ; Online: Therapeutic targeting of the pathological triad of extrasynaptic NMDA receptor signaling in neurodegenerations.

    Bading, Hilmar

    The Journal of experimental medicine

    2017  Volume 214, Issue 3, Page(s) 569–578

    Abstract: Activation of ... ...

    Abstract Activation of extrasynaptic
    MeSH term(s) Animals ; Calcium Signaling ; Cell Nucleus/metabolism ; Energy Metabolism ; Humans ; Neurodegenerative Diseases/drug therapy ; Neuroprotective Agents/therapeutic use ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors ; Receptors, N-Methyl-D-Aspartate/physiology ; Signal Transduction/drug effects ; Signal Transduction/physiology
    Chemical Substances Neuroprotective Agents ; Receptors, N-Methyl-D-Aspartate
    Language English
    Publishing date 2017-02-16
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20161673
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  4. Book ; Online ; Thesis: DNA methylation and transcriptional control in memory formation, persistence and suppression

    Kupke, Janina [Verfasser] / Bading, Hilmar [Akademischer Betreuer]

    2023  

    Author's details Janina Kupke ; Betreuer: Hilmar Bading
    Keywords Biowissenschaften, Biologie ; Life Science, Biology
    Subject code sg570
    Language English
    Publisher Universitätsbibliothek Heidelberg
    Publishing place Heidelberg
    Document type Book ; Online ; Thesis
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  5. Book ; Online ; Thesis: Apical Neural Stem Cells and the Effect of Growth/Differentiation Factor 15 on their Primary Cilia and Proliferation

    Baur, Katja [Verfasser] / Bading, Hilmar [Akademischer Betreuer]

    2023  

    Author's details Katja Baur ; Betreuer: Hilmar Bading
    Keywords Biowissenschaften, Biologie ; Life Science, Biology
    Subject code sg570
    Language English
    Publisher Universitätsbibliothek Heidelberg
    Publishing place Heidelberg
    Document type Book ; Online ; Thesis
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  6. Book ; Online ; Thesis: Development of axon-carrying dendrite cells in murine hippocampus and primary somatosensory cortex

    Lehmann, Nadja [Verfasser] / Bading, Hilmar [Akademischer Betreuer]

    2023  

    Author's details Nadja Lehmann ; Betreuer: Hilmar Bading
    Keywords Biowissenschaften, Biologie ; Life Science, Biology
    Subject code sg570
    Language English
    Publisher Universitätsbibliothek Heidelberg
    Publishing place Heidelberg
    Document type Book ; Online ; Thesis
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  7. Article: Pathophysiological Ionotropic Glutamate Signalling in Neuroinflammatory Disease as a Therapeutic Target.

    Fairless, Richard / Bading, Hilmar / Diem, Ricarda

    Frontiers in neuroscience

    2021  Volume 15, Page(s) 741280

    Abstract: Glutamate signalling is an essential aspect of neuronal communication involving many different glutamate receptors, and underlies the processes of memory, learning and synaptic plasticity. Despite neuroinflammatory diseases covering a range of maladies ... ...

    Abstract Glutamate signalling is an essential aspect of neuronal communication involving many different glutamate receptors, and underlies the processes of memory, learning and synaptic plasticity. Despite neuroinflammatory diseases covering a range of maladies with very different biological causes and pathophysiologies, a central role for dysfunctional glutamate signalling is becoming apparent. This is not just restricted to the well-described role of glutamate in mediating neurodegeneration, but also includes a myriad of other influences that glutamate can exert on the vasculature, as well as immune cell and glial regulation, reflecting the ability of neurons to communicate with these compartments in order to couple their activity with neuronal requirements. Here, we discuss the role of pathophysiological glutamate signalling in neuroinflammatory disease, using both multiple sclerosis and Alzheimer's disease as examples, and how current steps are being made to harness our growing understanding of these processes in the development of neuroprotective strategies. This review focuses in particular on
    Language English
    Publishing date 2021-10-21
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2021.741280
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  8. Article ; Online: Expression of the primate-specific LINC00473 RNA in mouse neurons promotes excitability and CREB-regulated transcription.

    Pruunsild, Priit / Bengtson, C Peter / Loss, Isabel / Lohrer, Benjamin / Bading, Hilmar

    The Journal of biological chemistry

    2023  Volume 299, Issue 5, Page(s) 104671

    Abstract: The LINC00473 (Lnc473) gene has previously been shown to be associated with cancer and psychiatric disorders. Its expression is elevated in several types of tumors and decreased in the brains of patients diagnosed with schizophrenia or major depression. ... ...

    Abstract The LINC00473 (Lnc473) gene has previously been shown to be associated with cancer and psychiatric disorders. Its expression is elevated in several types of tumors and decreased in the brains of patients diagnosed with schizophrenia or major depression. In neurons, Lnc473 transcription is strongly responsive to synaptic activity, suggesting a role in adaptive, plasticity-related mechanisms. However, the function of Lnc473 is largely unknown. Here, using a recombinant adeno-associated viral vector, we introduced a primate-specific human Lnc473 RNA into mouse primary neurons. We show that this resulted in a transcriptomic shift comprising downregulation of epilepsy-associated genes and a rise in cAMP response element-binding protein (CREB) activity, which was driven by augmented CREB-regulated transcription coactivator 1 nuclear localization. Moreover, we demonstrate that ectopic Lnc473 expression increased neuronal excitability as well as network excitability. These findings suggest that primates may possess a lineage-specific activity-dependent modulator of CREB-regulated neuronal excitability.
    MeSH term(s) Animals ; Humans ; Mice ; Cyclic AMP Response Element-Binding Protein/metabolism ; Epilepsy/genetics ; Neurons/metabolism ; Primates/genetics
    Chemical Substances Creb1 protein, mouse ; Crtc1 protein, mouse ; Cyclic AMP Response Element-Binding Protein ; LINC00473 RNA, human
    Language English
    Publishing date 2023-04-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.104671
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    Uc I Zs.108: Show issues Location:
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  9. Article ; Online: Nuclear calcium signalling in the regulation of brain function.

    Bading, Hilmar

    Nature reviews. Neuroscience

    2013  Volume 14, Issue 9, Page(s) 593–608

    Abstract: Synaptic activity initiates biochemical processes that have various outcomes, including the formation of memories, increases in neuronal survival and the development of chronic pain and addiction. Virtually all activity-induced, long-lasting adaptations ... ...

    Abstract Synaptic activity initiates biochemical processes that have various outcomes, including the formation of memories, increases in neuronal survival and the development of chronic pain and addiction. Virtually all activity-induced, long-lasting adaptations of brain functions require a dialogue between synapses and the nucleus that results in changes in gene expression. Calcium signals that are induced by synaptic activity and propagate into the nucleus are a major route for synapse-to-nucleus communication. Recent findings indicate that diverse forms of neuroadaptation require calcium transients in the nucleus to switch on the necessary genomic programme. Deficits in nuclear calcium signalling as a result of a reduction in synaptic activity or increased extrasynaptic NMDA receptor signalling may underlie the aetiologies of various diseases, including neurodegeneration and cognitive dysfunction.
    MeSH term(s) Animals ; Brain/physiology ; Calcium/metabolism ; Calcium Signaling/physiology ; Cell Nucleus/metabolism ; Humans ; Nerve Degeneration/metabolism ; Nerve Degeneration/physiopathology ; Neurons/metabolism ; Synapses/metabolism
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2013-08-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2034150-7
    ISSN 1471-0048 ; 1471-0048 ; 1471-003X
    ISSN (online) 1471-0048
    ISSN 1471-0048 ; 1471-003X
    DOI 10.1038/nrn3531
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  10. Article ; Online: Shaping the human brain: evolutionary cis-regulatory plasticity drives changes in synaptic activity-controlled adaptive gene expression.

    Pruunsild, Priit / Bading, Hilmar

    Current opinion in neurobiology

    2019  Volume 59, Page(s) 34–40

    Abstract: Neuronal activity-induced gene expression programs involved in synaptic structure- and plasticity-related functions are similar in mice and humans, yet bear distinct features. These include gains or losses of activity-responsiveness of certain genes and ... ...

    Abstract Neuronal activity-induced gene expression programs involved in synaptic structure- and plasticity-related functions are similar in mice and humans, yet bear distinct features. These include gains or losses of activity-responsiveness of certain genes and differences in gene induction profiles. Here, we discuss a possible origin of dissimilarities in activity-regulated transcription between species. We highlight that while synapse-to-nucleus signalling pathways are evolutionarily conserved, cis-regulatory plasticity has been driving species-specific remodelling of the activity-controlled enhancer landscape, thereby affecting gene regulation. In particular, evolutionary rearrangements of transcription factor binding site placements together with potential species-dependent developmental stage- and/or cell type-specific epigenetic and other trans-acting mechanisms are most likely at least in part accountable for between-species diversity in activity-regulated transcription. It is conceivable that cis-regulatory plasticity may have equipped the synaptic activity-driven adaptive gene program in human neurons with unique, species-specific qualities.
    MeSH term(s) Animals ; Brain ; Gene Expression Regulation ; Gene Expression Regulation, Developmental ; Humans ; Mice ; Neurons ; Signal Transduction
    Language English
    Publishing date 2019-05-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1078046-4
    ISSN 1873-6882 ; 0959-4388
    ISSN (online) 1873-6882
    ISSN 0959-4388
    DOI 10.1016/j.conb.2019.04.003
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