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Bading group

Principal investigator:
Universität Heidelberg
Im Neuenheimer Feld 364
69121 Heidelberg


General research interests and goals:

Our laboratory studies the role of calcium signaling pathways activated by synaptic and extrasynaptic NMDA receptors in activity–regulated gene expression and neuroadaptations. Synaptic NMDA receptors trigger synapse-to-nucleus signaling leading to genomic responses important for physiological processes, in particular learning and memory and acquired neuroprotection. In contrast, extrasynaptic NMDA receptor signaling causes neurodegeneration and cell death. This process is mediated by a pathological triad consisting of mitochondrial dysfunction, loss of integrity of neuronal structures and connectivity, and disruption of excitation-transcription that is common to many neurodegenerative diseases.


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Current group members:

PostDocs: Dr. Anna Hagenston Hertle
PhD students: Konstantinos Xylouris
Associates: Markus Breit

Key publications:

Bas-Orth C, Tan YW, Lau D, Bading H (2017) Synaptic activity drives a genomic program that promotes a neuronal Warburg effect J. Biol. Chem. in press .
Bas-Orth C, Tan YW, Oliveira AM, Bengtson CP, Bading H (2016) The calmodulin-binding transcription factor is required for long-term memory formation in mice Learning & Memory 23, 313-321 .
Mauceri D, Hagenston AM, Schramm K, Weiss U, Bading H (2015) Nuclear calcium buffering capacity shapes neuronal architecture J. Biol. Chem. 290, 23039-23049 .
Qiu J, Tan YW, Hagenston AM, Martel MA, Kneisel N, Skehel PA, Wyllie DJ, Bading H, Hardingham GE (2013) Mitochondrial calcium uniporter Mcu controls excitotoxicity and is repressed by neuroprotective nuclear calcium signals Nat. Commun. 4:2034 doi: 10.1038/ncomms3034 .
Bas-Orth C, Bading H (2012) The divergence-convergence model of acquired neuroprotection Mech. Dev. 130, 396-401 .