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Guy C.-K. Chan

Researcher at University of Washington

Publications -  37
Citations -  4054

Guy C.-K. Chan is an academic researcher from University of Washington. The author has contributed to research in topics: Adenylyl cyclase & Long-term potentiation. The author has an hindex of 27, co-authored 37 publications receiving 3795 citations. Previous affiliations of Guy C.-K. Chan include Washington University in St. Louis & Saint Louis University.

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Cross Talk between ERK and PKA Is Required for Ca2+ Stimulation of CREB-Dependent Transcription and ERK Nuclear Translocation

TL;DR: It is reported that extracellular signal-related protein kinase (ERK) signaling is obligatory for Ca2+-stimulated transcription in PC12 cells and hippocampal neurons and suggests that the activation of CREB by ERK plays a critical role in the formation of long lasting neuronal plasticity.
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Disruption of the type III adenylyl cyclase gene leads to peripheral and behavioral anosmia in transgenic mice.

TL;DR: Interestingly, electroolfactogram responses stimulated by either cAMP- or inositol 1,4,5-triphosphate- (IP3-) inducing odorants were completely ablated in AC3 mutants, despite the presence of AC2 and AC4 in olfactory cilia, indicating that AC3 and cAMP signaling are critical for olfaction-dependent behavior.
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Circadian oscillation of hippocampal MAPK activity and cAMP: Implications for memory persistence

TL;DR: The data suggest that the persistence of long-term memories may depend on reactivation of the cAMP/MAPK/CREB transcriptional pathway in the hippocampus during the circadian cycle.
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Hippocampal Neurotoxicity of Δ9-Tetrahydrocannabinol

TL;DR: It is reported that Δ9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, is toxic for hippocampal neurons and hypothesize that THC neurotoxicity is attributable to activation of the prostanoid synthesis pathway and generation of free radicals by cyclooxygenase.
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Phosphorylation and inhibition of olfactory adenylyl cyclase by CaM kinase II in Neurons: a mechanism for attenuation of olfactory signals.

TL;DR: A polyclonal antibody specific for AC3 phosphorylation was generated and blocked by inhibitors of CaMKII, which also ablated cAMP decreases associated with odorant-stimulated cAMP transients, defining a novel mechanism for termination of olfactory signaling that may be important in olfaction responses.