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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10.1074/jbc.M112.415141

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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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EP - 10307

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 15

ER -

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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