Philip E. Chen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Philip E. Chen has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
- Alexander J. Annala
Department of Neuroscience, City of Hope National Medical Center, Beckman Research Institute, Duarte, CA, USA
1 shared publication Cezar M. Tigaret
Laboratory for Molecular Pharmacology, University College London, London WC1E 6BT, United Kingdom
1 shared publication- Christian G. Specht
Neuro-Bicêtre, Inserm U1195, Université Paris-Saclay
1 shared publication Georg F. Rast
Laboratory for Molecular Pharmacology, University College London, London WC1E 6BT, United Kingdom
1 shared publicationGeorge Dickson
Centres of Gene and Cell Therapy and Biomedical Sciences, Department of Biological Sciences, Royal Holloway University of London, Egham, Surrey, UK
1 shared publicationGuiquan Chen
Laboratory for Cognitive Neuroscience, Centre for Cognitive and Neural Systems, University of Edinburgh, Edinburgh EH8 9JZ, United Kingdom
1 shared publication
Latest Publications
- Open Access
- 16 September 2021
- Published by Elsevier in Journal of Neuroscience Methods
- Vol. 364, 109357
A new strategy to increase RNA editing at the Q/R site of GluA2 AMPA receptor subunits by targeting alternative splicing patterns of ADAR2
- 16 September 2021
- Published by Elsevier in Journal of Neuroscience Methods
- Vol. 364, 109357
Open AccessA new strategy to increase RNA editing at the Q/R site of GluA2 AMPA receptor subunits by targeting alternative splicing patterns of ADAR2
- Open Access
- 11 May 2019
- Published by Wiley in FEBS Letters
- Vol. 593 (12) , 1381-1391
Overexpression of the dopamine receptor‐interacting protein Alix/AIP1 modulates NMDA receptor‐triggered cell death
Alix/AIP1 is an adaptor protein involved in apoptosis, endocytic membrane trafficking and brain development. Alix has been found within the human postsynaptic density (PSD) and, since NMDA receptors (NMDARs) are central components of the PSD, we hypothesized that the close proximity of both proteins may allow Alix to influence the downstream pathways following NMDAR activation. NMDARs play important roles in excitotoxicity and we evaluated the effects of recombinant Alix in an NMDAR cell death assay. Overexpression of Alix with NMDARs increases the potency of NMDAR‐ induced cell death compared to cells expressing only NMDARs, and this requires expression of the Alix C‐terminal region. Therefore, we demonstrate a previously unreported role for Alix as a potential modulator of NMDAR function.
- 11 May 2019
- Published by Wiley in FEBS Letters
- Vol. 593 (12) , 1381-1391
Open AccessOverexpression of the dopamine receptor‐interacting protein Alix/AIP1 modulates NMDA receptor‐triggered cell death
Alix/AIP1 is an adaptor protein involved in apoptosis, endocytic membrane trafficking and brain development. Alix has been found within the human postsynaptic density (PSD) and, since NMDA receptors (NMDARs) are central components of the PSD, we hypothesized that the close proximity of both proteins may allow Alix to influence the downstream pathways following NMDAR activation. NMDARs play important roles in excitotoxicity and we evaluated the effects of recombinant Alix in an NMDAR cell death assay. Overexpression of Alix with NMDARs increases the potency of NMDAR‐ induced cell death compared to cells expressing only NMDARs, and this requires expression of the Alix C‐terminal region. Therefore, we demonstrate a previously unreported role for Alix as a potential modulator of NMDAR function.
- 30 September 2009
- Published by Cold Spring Harbor Laboratory in Learning & Memory
- Vol. 16 (10) , 635-644
Behavioral deficits and subregion-specific suppression of LTP in mice expressing a population of mutant NMDA receptors throughout the hippocampus
The NMDA receptor (NMDAR) subunit GluN1 is an obligatory component of NMDARs without a known functional homolog and is expressed in almost every neuronal cell type. The NMDAR system is a coincidence detector with critical roles in spatial learning and synaptic plasticity. Its coincidence detection property is crucial for the induction of hippocampal long-term potentiation (LTP). We have generated a mutant mouse model expressing a hypomorph of the Grin1N598R allele, which leads to a minority (about 10%) of coincidence detection-impaired NMDARs. Surprisingly, these animals revealed specific functional changes in the dentate gyrus (DG) of the hippocampal formation. Early LTP was expressed normally in area CA1 in vivo, but was completely suppressed at perforant path-granule cell synapses in the DG. In addition, there was a pronounced reduction in the amplitude of the evoked population spike in the DG. These specific changes were accompanied by behavioral impairments in spatial recognition, spatial learning, reversal learning, and retention. Our data show that minor changes in GluN1-dependent NMDAR physiology can cause dramatic consequences in synaptic signaling in a subregion-specific fashion despite the nonredundant nature of the GluN1 gene and its global expression.
- 30 September 2009
- Published by Cold Spring Harbor Laboratory in Learning & Memory
- Vol. 16 (10) , 635-644
Behavioral deficits and subregion-specific suppression of LTP in mice expressing a population of mutant NMDA receptors throughout the hippocampus
The NMDA receptor (NMDAR) subunit GluN1 is an obligatory component of NMDARs without a known functional homolog and is expressed in almost every neuronal cell type. The NMDAR system is a coincidence detector with critical roles in spatial learning and synaptic plasticity. Its coincidence detection property is crucial for the induction of hippocampal long-term potentiation (LTP). We have generated a mutant mouse model expressing a hypomorph of the Grin1N598R allele, which leads to a minority (about 10%) of coincidence detection-impaired NMDARs. Surprisingly, these animals revealed specific functional changes in the dentate gyrus (DG) of the hippocampal formation. Early LTP was expressed normally in area CA1 in vivo, but was completely suppressed at perforant path-granule cell synapses in the DG. In addition, there was a pronounced reduction in the amplitude of the evoked population spike in the DG. These specific changes were accompanied by behavioral impairments in spatial recognition, spatial learning, reversal learning, and retention. Our data show that minor changes in GluN1-dependent NMDAR physiology can cause dramatic consequences in synaptic signaling in a subregion-specific fashion despite the nonredundant nature of the GluN1 gene and its global expression.