Bad Ac-etylated Tau

Jane C. Hettinger; John R. Cirrito

doi:10.1016/j.neuron.2016.04.008

Bad Ac-etylated Tau

Jane C. Hettinger, John R. Cirrito

Research output: Contribution to journal › Short survey › peer-review

5 Scopus citations

Abstract

By using a tau construct with two mimicked acetylation sites as identified in AD brains, Tracy et al. (2016) found that acetylated tau promotes synaptic dysfunction through disruption of postsynaptic KIBRA signaling pathways, actin dynamics, and AMPA receptor trafficking. By using a tau construct with two mimicked acetylation sites as identified in AD brains, Tracy et al. found that acetylated tau promotes synaptic dysfunction through disruption of postsynaptic KIBRA signaling pathways, actin dynamics, and AMPA receptor trafficking.

Original language	English
Pages (from-to)	205-206
Number of pages	2
Journal	Neuron
Volume	90
Issue number	2
DOIs	https://doi.org/10.1016/j.neuron.2016.04.008
State	Published - Apr 20 2016

Keywords

Acetylation
Alzheimer's disease
KIBRA
Post-translational modification
Tau
Tauopathy

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10.1016/j.neuron.2016.04.008

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title = "Bad Ac-etylated Tau",

abstract = "By using a tau construct with two mimicked acetylation sites as identified in AD brains, Tracy et al. (2016) found that acetylated tau promotes synaptic dysfunction through disruption of postsynaptic KIBRA signaling pathways, actin dynamics, and AMPA receptor trafficking. By using a tau construct with two mimicked acetylation sites as identified in AD brains, Tracy et al. found that acetylated tau promotes synaptic dysfunction through disruption of postsynaptic KIBRA signaling pathways, actin dynamics, and AMPA receptor trafficking.",

keywords = "Acetylation, Alzheimer's disease, KIBRA, Post-translational modification, Tau, Tauopathy",

author = "Hettinger, {Jane C.} and Cirrito, {John R.}",

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AU - Cirrito, John R.

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AB - By using a tau construct with two mimicked acetylation sites as identified in AD brains, Tracy et al. (2016) found that acetylated tau promotes synaptic dysfunction through disruption of postsynaptic KIBRA signaling pathways, actin dynamics, and AMPA receptor trafficking. By using a tau construct with two mimicked acetylation sites as identified in AD brains, Tracy et al. found that acetylated tau promotes synaptic dysfunction through disruption of postsynaptic KIBRA signaling pathways, actin dynamics, and AMPA receptor trafficking.

KW - Acetylation

KW - Alzheimer's disease

KW - KIBRA

KW - Post-translational modification

KW - Tau

KW - Tauopathy

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JO - Neuron

JF - Neuron

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ER -

Bad Ac-etylated Tau

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Keywords

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