D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 46 Citations 12,251 95 World Ranking 12187 National Ranking 976

Research.com Recognitions

Awards & Achievements

2018 - Fellow of the Royal Society of Edinburgh

Fellow of The Academy of Medical Sciences, United Kingdom

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Neuron
  • Genetics

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.

His most cited work include:

  • Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways (1308 citations)
  • Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders (1021 citations)
  • Distinct functions of nuclear and cytoplasmic calcium in the control of gene expression (669 citations)

What are the main themes of his work throughout his whole career to date?

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.

He most often published in these fields:

  • Cell biology (43.59%)
  • Neuroscience (37.82%)
  • NMDA receptor (28.85%)

What were the highlights of his more recent work (between 2018-2021)?

  • Cell biology (43.59%)
  • Neuroscience (37.82%)
  • Amyotrophic lateral sclerosis (5.77%)

In recent papers he was focusing on the following fields of study:

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.

Between 2018 and 2021, his most popular works were:

  • Deletion of a Csf1r enhancer selectively impacts CSF1R expression and development of tissue macrophage populations. (50 citations)
  • GRIN2A-related disorders : genotype and functional consequence predict phenotype (50 citations)
  • Amyloid Beta and Tau Cooperate to Cause Reversible Behavioral and Transcriptional Deficits in a Model of Alzheimer's Disease. (35 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Neuron
  • Genetics

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.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

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)

1728 Citations

Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders

Giles E. Hardingham;Hilmar Bading.
Nature Reviews Neuroscience (2010)

1335 Citations

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)

847 Citations

The Yin and Yang of NMDA receptor signalling.

Giles E. Hardingham;Hilmar Bading.
Trends in Neurosciences (2003)

802 Citations

Nuclear calcium signaling controls CREB-mediated gene expression triggered by synaptic activity.

Giles E. Hardingham;Fiona J. L. Arnold;Hilmar Bading.
Nature Neuroscience (2001)

579 Citations

Synaptic NMDA receptor activity boosts intrinsic antioxidant defenses

Sofia Papadia;Francesc X Soriano;Frédéric Léveillé;Marc-Andre Martel.
Nature Neuroscience (2008)

534 Citations

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)

524 Citations

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)

336 Citations

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)

332 Citations

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)

331 Citations

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