NDLI: Amyloid β Regulates the Expression and Function of AIP1

Content Provider	Springer Nature Link
Author	Wang, Huaiming Fan, Lijing Wang, Hong Ma, Xixin Du, Zhongde
Copyright Year	2014
Abstract	Apoptosis signal-regulating kinase 1–interacting (ASK1-interacting) protein-1 (AIP1) is a newly identified novel member of the Ras GTPase-activating protein family, which has been implicated in cell growth inhibition and cell apoptosis. However, the effects of AIP1 in Alzheimer’s disease (AD) are unknown. In the present study, we found that AIP1 was elevated in the brain of AD Tg2576 mice and Aβ1-42 treated brain cerebral microvascular endothelial cells (CECs). Aβ1-42 treatment induced the interaction of AIP1 and apoptosis signal-regulating kinase 1 (ASK1), which led to dissociation of ASK1 and its inhibitor 14-3-3. Dissociation of ASK1 from 14-3-3 leads to ASK1 activation. Indeed, Aβ1-42 dephosphorylated ASK1 at Ser-967, suggesting that Aβ1-42 increased ASK1 activity. Importantly, disassociation of ASK1 and 14-3-3 induced by Aβ1–42 could be rescued by silence of AIP1. In addition, down-regulation of AIP1 also led to attenuation of the activation of JNK, as well as p53, downstream signaling targets of ASK1. AIP1 silencing attenuated the pro-apoptotic effects of Aβ1-42 on CECs. We propose that AIP1 mediates Aβ induced ASK1 activation by facilitating dissociation of 14-3-3, suggesting a novel mechanism for Aβ-induced apoptosis in CECs.
Starting Page	227
Ending Page	232
Page Count	6
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	55
Issue Number	1
e-ISSN	15591166
Language	English
Publisher	Springer US
Publisher Date	2014-07-02
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Alzheimer’s disease Aβ1-42 Apoptosis signal-regulating kinase 1–interacting (ASK1-interacting) protein-1 (AIP1) Apoptosis signal-regulating kinase 1 (ASK1) Apoptosis Neurosciences Neurochemistry Cell Biology Proteomics Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

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