2018 - Fellow of the Royal Society of Edinburgh
Fellow of The Academy of Medical Sciences, United Kingdom
Neuroscience, NMDA receptor, CREB, Cell biology and Neuroprotection are his primary areas of study. He works on Neuroscience which deals in particular with Stimulation. The various areas that Giles E. Hardingham examines in his NMDA receptor study include Glutamate receptor, Signal transduction and Programmed cell death.
His study looks at the relationship between Signal transduction and fields such as Neuron, as well as how they intersect with chemical problems. While the research belongs to areas of CREB, he spends his time largely on the problem of Molecular biology, intersecting his research to questions surrounding Patch clamp, Disks Large Homolog 4 Protein, Transfection and Phosphorylation. His Cell biology study integrates concerns from other disciplines, such as Voltage-dependent calcium channel, Transcription factor, Gene expression and Biochemistry.
Giles E. Hardingham mainly focuses on Cell biology, Neuroscience, NMDA receptor, Neuroprotection and Signal transduction. His Cell biology research is multidisciplinary, incorporating perspectives in Gene expression, Transcription factor, CREB, Biochemistry and Regulation of gene expression. His research integrates issues of Calcium and Cell type in his study of Gene expression.
The Neuroscience study combines topics in areas such as Cellular differentiation, Neurodegeneration, Neurotransmission and Induced pluripotent stem cell. His NMDA receptor research incorporates elements of Glutamate receptor, Synaptic plasticity and Synaptogenesis. His research links Programmed cell death with Neuroprotection.
His scientific interests lie mostly in Cell biology, Neuroscience, Amyotrophic lateral sclerosis, NMDA receptor and Neurodegeneration. Giles E. Hardingham interconnects Induced pluripotent stem cell, Premovement neuronal activity and Chromosomal translocation in the investigation of issues within Cell biology. His work in the fields of Neuroscience, such as Cognition, overlaps with other areas such as Astrocyte.
His study in Amyotrophic lateral sclerosis is interdisciplinary in nature, drawing from both Meta-analysis and Oncology. NMDA receptor is a subfield of Receptor that he explores. His Signal transduction study combines topics from a wide range of disciplines, such as Transcriptome and Cell type.
Giles E. Hardingham spends much of his time researching Neuroscience, Mutation, Synaptogenesis, Cell biology and Microglia. He works in the field of Neuroscience, focusing on Effects of sleep deprivation on cognitive performance in particular. His studies deal with areas such as Motor neuron, Mutant and Induced pluripotent stem cell as well as Mutation.
His Synaptogenesis research is multidisciplinary, relying on both NMDA receptor, Excitotoxicity, Scaffold protein, Protein subunit and Neurodegeneration. His NMDA receptor research includes elements of Synaptic plasticity, Glutamate receptor, Dendritic spine, Neurogenesis and Patch clamp. Giles E. Hardingham combines subjects such as Embryonic stem cell, Transcriptome, Cell division and Cell growth with his study of Cell biology.
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Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways
Giles E. Hardingham;Yuko Fukunaga;Hilmar Bading;Hilmar Bading.
Nature Neuroscience (2002)
Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders
Giles E. Hardingham;Hilmar Bading.
Nature Reviews Neuroscience (2010)
Distinct functions of nuclear and cytoplasmic calcium in the control of gene expression
Giles E. Hardingham;Sangeeta Chawla;Claire M. Johnson;Hilmar Bading.
Nature (1997)
The Yin and Yang of NMDA receptor signalling.
Giles E. Hardingham;Hilmar Bading.
Trends in Neurosciences (2003)
Nuclear calcium signaling controls CREB-mediated gene expression triggered by synaptic activity.
Giles E. Hardingham;Fiona J. L. Arnold;Hilmar Bading.
Nature Neuroscience (2001)
Synaptic NMDA receptor activity boosts intrinsic antioxidant defenses
Sofia Papadia;Francesc X Soriano;Frédéric Léveillé;Marc-Andre Martel.
Nature Neuroscience (2008)
CBP: A Signal-Regulated Transcriptional Coactivator Controlled by Nuclear Calcium and CaM Kinase IV
Sangeeta Chawla;Giles E. Hardingham;David R. Quinn;Hilmar Bading.
Science (1998)
Mutant induced pluripotent stem cell lines recapitulate aspects of TDP-43 proteinopathies and reveal cell-specific vulnerability
Bilada Bilican;Andrea Serio;Sami J. Barmada;Agnes Lumi Nishimura.
Proceedings of the National Academy of Sciences of the United States of America (2012)
A calcium microdomain near NMDA receptors: on switch for ERK-dependent synapse-to-nucleus communication
Giles E. Hardingham;Fiona J. L. Arnold;Hilmar Bading.
Nature Neuroscience (2001)
Control of Recruitment and Transcription-Activating Function of CBP Determines Gene Regulation by NMDA Receptors and L-Type Calcium Channels
Giles E. Hardingham;Sangeeta Chawla;Francisco H. Cruzalegui;Hilmar Bading.
Neuron (1999)
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