scispace - formally typeset
W

Weihong Tu

Researcher at University of Central Florida

Publications -  5
Citations -  1142

Weihong Tu is an academic researcher from University of Central Florida. The author has contributed to research in topics: AMPA receptor & Glutamate receptor. The author has an hindex of 5, co-authored 5 publications receiving 1042 citations. Previous affiliations of Weihong Tu include Louisiana State University.

Papers
More filters
Journal ArticleDOI

DAPK1 Interaction with NMDA Receptor NR2B Subunits Mediates Brain Damage in Stroke

TL;DR: C cerebral ischemia recruits death-associated protein kinase 1 (DAPK1) into the NMDA receptor NR2B protein complex in the cortex of adult mice and this interaction acts as a central mediator for stroke damage.
Journal ArticleDOI

Deregulation of HDAC1 by p25/Cdk5 in Neurotoxicity

TL;DR: This work shows that deregulation of histone deacetylase 1 (HDAC1) activity by p25/Cdk5 induces aberrant cell-cycle activity and double-strand DNA breaks leading to neurotoxicity, and outlines a pathological signaling pathway illustrating the importance of maintaining HDAC1 activity in the adult neuron.
Journal ArticleDOI

ADAR2-Dependent RNA Editing of AMPA Receptor Subunit GluR2 Determines Vulnerability of Neurons in Forebrain Ischemia

TL;DR: It is shown that forebrain ischemia in adult rats selectively reduces expression of ADAR2 enzyme and, hence, disrupts RNA Q/R site editing of GluR2 subunit in vulnerable neurons, which determines vulnerability of neurons in the rat hippocampus to fore brain ischemic insult.
Journal ArticleDOI

EPAC null mutation impairs learning and social interactions via aberrant regulation of miR-124 and Zif268 translation

TL;DR: It is shown that EPAC null mutation impairs long-term potentiation (LTP) and that this impairment is paralleled with the severe deficits in spatial learning and social interactions and is mediated in a direct manner by miR-124 transcription and Zif268 translation.
Journal ArticleDOI

Expression of functional Kir6.1 channels regulates glutamate release at CA3 synapses in generation of epileptic form of seizures.

TL;DR: Whole‐cell patch clamp recordings demonstrate that genetic deletion of the Kir6.1/SUR1 channels enhances glutamate release at CA3 synapses and inhibits seizure responses and possibly acts via limiting excitatory glutamate release.