Β2 adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

Dayong Wang; Qin Fu; Yuan Zhou; Bing Xu; Qian Shi; Benedict Igwe; Lucas Matt; Johannes W. Hell; Elena V. Wisely; Salvatore Oddo; Yang K. Xiang

doi:10.1074/jbc.M112.415141

Β₂ adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

Dayong Wang, Qin Fu, Yuan Zhou, Bing Xu, Qian Shi, Benedict Igwe, Lucas Matt, Johannes W. Hell, Elena V. Wisely, Salvatore Oddo, Yang K. Xiang

Research output: Contribution to journal › Article › peer-review

88 Scopus citations

Abstract

Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β₂AR independently of presynaptic activities. Results: β₂AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β₂AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β₂ARs.

Original language	English (US)
Pages (from-to)	10298-10307
Number of pages	10
Journal	Journal of Biological Chemistry
Volume	288
Issue number	15
DOIs	https://doi.org/10.1074/jbc.M112.415141
State	Published - Apr 12 2013
Externally published	Yes

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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Wang, D., Fu, Q., Zhou, Y., Xu, B., Shi, Q., Igwe, B., Matt, L., Hell, J. W., Wisely, E. V., Oddo, S., & Xiang, Y. K. (2013). Β₂ adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models. Journal of Biological Chemistry, 288(15), 10298-10307. https://doi.org/10.1074/jbc.M112.415141

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title = "Β2 adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models",

abstract = "Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β2AR independently of presynaptic activities. Results: β2AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β2AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β2ARs.",

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doi = "10.1074/jbc.M112.415141",

language = "English (US)",

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T1 - Β2 adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

AU - Wang, Dayong

AU - Fu, Qin

AU - Zhou, Yuan

AU - Xu, Bing

AU - Shi, Qian

AU - Igwe, Benedict

AU - Matt, Lucas

AU - Hell, Johannes W.

AU - Wisely, Elena V.

AU - Oddo, Salvatore

AU - Xiang, Yang K.

PY - 2013/4/12

Y1 - 2013/4/12

N2 - Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β2AR independently of presynaptic activities. Results: β2AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β2AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β2ARs.

AB - Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β2AR independently of presynaptic activities. Results: β2AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β2AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β2ARs.

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Β₂ adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

Abstract

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