Kinase–Kinase Interaction and Modulation of Tau Phosphorylation

Hashiguchi, Mitsuko; Hashiguchi, Takashi

doi:10.1016/b978-0-12-405210-9.00004-7

Cited by 35 publications

(21 citation statements)

References 146 publications

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“…However, recent studies show that TAU is also expressed in glial cells (Fuster-Matanzo et al, 2012). The phosphorylation of TAU regulates microtubule binding and assembly, but hyperphosphorylation destabilizes microtubules by decreased binding of TAU to microtubules (Hashiguchi and Hashiguchi, 2013). This results in aggregation of the protein leading to the formation of neurofibrillary tangles (Gotz et al, 2013), a pathological feature in most neurodegenerative diseases, especially AD.…”

Section: Tau Hyperphosphorylationmentioning

confidence: 98%

Chronic stress as a risk factor for Alzheimer’s disease

Machado¹,

Herrera²,

Pablos³

et al. 2014

Reviews in the Neurosciences

151

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AbstractThis review aims to point out that chronic stress is able to accelerate the appearance of Alzheimer’s disease (AD), proposing the former as a risk factor for the latter. Firstly, in the introduction we describe some human epidemiological studies pointing out the possibility that chronic stress could increase the incidence, or the rate of appearance of AD. Afterwards, we try to justify these epidemiological results with some experimental data. We have reviewed the experiments studying the effect of various stressors on different features in AD animal models. Moreover, we also point out the data obtained on the effect of chronic stress on some processes that are known to be involved in AD, such as inflammation and glucose metabolism. Later, we relate some of the processes known to be involved in aging and AD, such as accumulation of β-amyloid, TAU hyperphosphorylation, oxidative stress and impairement of mitochondrial function, emphasizing how they are affected by chronic stress/glucocorticoids and comparing with the description made for these processes in AD. All these data support the idea that chronic stress could be considered a risk factor for AD.

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Section: Tau Hyperphosphorylationmentioning

confidence: 98%

Chronic stress as a risk factor for Alzheimer’s disease

Machado¹,

Herrera²,

Pablos³

et al. 2014

Reviews in the Neurosciences

151

View full text Add to dashboard Cite

show abstract

“…The three tau kinases, GSK-3β, CDK-5, and PKA, associate with both tau and microtubules. Although they show a wide spectrum of phosphorylation, the major phosphorylatable sites of tau for each kinase are limited in preference (Hashiguchi and Hashiguchi, 2013). Multisite phosphorylation occurs in PHF-tau and is explained by the catalytic activities of the different kinases, although the functional significance of this phenomenon is not completely understood.…”

Section: Gsk-3β As a Molecular Link Between Aβ And Taumentioning

confidence: 99%

“…A moderate phosphorylation of Ser46, Thr50, and Ser202/Thr205 has also been reported (Illenberger et al, 1998), and minor phosphorylation of other residues has been described (Hanger et al, 2007). A complete description of these phosphorylation sites is provided in an extensive review by Hashiguchi and Hashiguchi (2013).…”

Section: Gsk-3β As a Molecular Link Between Aβ And Taumentioning

confidence: 99%

GSK-3Î², a pivotal kinase in Alzheimer disease

Llorens‐Martin¹,

Jurado

Hernández

et al. 2014

Front. Mol. Neurosci.

343

338

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Alzheimer disease (AD) is the most common form of age-related dementia. The etiology of AD is considered to be multifactorial as only a negligible percentage of cases have a familial or genetic origin. Glycogen synthase kinase-3 (GSK-3) is regarded as a critical molecular link between the two histopathological hallmarks of the disease, namely senile plaques and neurofibrillary tangles. In this review, we summarize current data regarding the involvement of this kinase in several aspects of AD development and progression, as well as key observations highlighting GSK-3 as one of the most relevant targets for AD treatment.

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“…Tau has multiple phosphorylation sites, and the numerous phosphorylated forms have different functions. Tau phosphorylation may affect microtubule stability and axonal transport, dendritic positioning and synaptic health, cell signaling at plasma membranes, protection of DNA from cell stressors, tau release and pathologic propagation (35). In this study, total Tau was identified to be upregulated, yet the specific phosphorylation sites remain to be further explored.…”

mentioning

confidence: 86%

A proteomics study of hyperhomocysteinemia injury of the hippocampal neurons using iTRAQ

Fang

Wang

Yan

et al. 2014

Molecular Medicine Reports

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Abstract. High levels of homocysteine, caused by abnormal methionine metabolism, can induce degeneration of mouse hippocampal neurons. iTRAQ™ technology has been widely used in the field of proteomics research and through employing this technology, the present study identified that hyperhomocysteinemia induced the downregulation of 52 proteins and upregulation of 44 proteins in the mouse hippocampus. Through gene ontology and pathway analysis, the upregulation of components of the cytoskeleton, actin, regulators of focal adhesion, calcium signaling pathways, tight junctions, ErbB and gonadotrophin-releasing hormone signaling, leukocyte, transendothelial migration, propanoate and pyruvate metabolism, valine, leucine and isoleucine biosynthesis, synthesis and degradation of ketone bodies and benzoate degradation via CoA ligation pathway, was identified. It was additionally verified that tau protein was highly expressed in the hyperhomocysteinemic neurons. Further analysis revealed that tau network proteins played functional roles in homocysteine-induced neuronal damage.

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Kinase–Kinase Interaction and Modulation of Tau Phosphorylation

Cited by 35 publications

References 146 publications

Chronic stress as a risk factor for Alzheimer’s disease

Chronic stress as a risk factor for Alzheimer’s disease

GSK-3Î², a pivotal kinase in Alzheimer disease

A proteomics study of hyperhomocysteinemia injury of the hippocampal neurons using iTRAQ

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