Jonathan Aow
University of California, San Diego
10 Papers
18 Citations
Jonathan Aow is an academic researcher from University of California, San Diego. The author has contributed to research in topics: NMDA receptor & Long-term depression. The author has an hindex of 6, co-authored 7 publications. Previous affiliations of Jonathan Aow include Genome Institute of Singapore.
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Papers
Metabotropic NMDA receptor function is required for NMDA receptor-dependent long-term depression
Sadegh Nabavi,Helmut W. Kessels,Helmut W. Kessels,Stephanie Alfonso,Jonathan Aow,Rocky Fox,Roberto Malinow +6 more
TL;DR: The findings indicate that metabotropic actions of NMDARs can weaken active synapses without raising postsynaptic calcium, thereby revising and expanding the mechanisms controlling synaptic plasticity.
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Agonist binding to the NMDA receptor drives movement of its cytoplasmic domain without ion flow.
TL;DR: This study demonstrates that transmembrane information transfer through the NMDAR is possible in the absence of ion flow through the receptor, and indicates that extracellular ligand binding to the N MDAR can transmit conformational information into the cell in the presence of ions.
104
Conformational signaling required for synaptic plasticity by the NMDA receptor complex
TL;DR: This study directly measures metabotropic signaling actions by NMDARs and provides insights into the mechanisms of synaptic depression, as well as monitoring agonist-driven conformational signaling at the N MDAR complex required for synaptic plasticity.
95
GluA1 trafficking and metabotropic NMDA: addressing results from other laboratories inconsistent with ours
TL;DR: Using rectification index as a measure of synaptic delivery of GluA1, it is not possible to conclude that 7CK is effective in blocking LTD from their type of experiment, and the methodology has complex effects on synaptic transmission.
35
Differential binding of the related transcription factors Pho4 and Cbf1 can tune the sensitivity of promoters to different levels of an induction signal
TL;DR: Ch Chromatin immunoprecipitation and computational analyses of natural Pho4 target genes, along with the activities of the reporter constructs, indicates that genes differ in their sensitivity to intermediate induction signals in part because of differences in their affinity for Cbf1.