Pin1 colocalization with phosphorylated tau in Alzheimer's disease and other tauopathies

Ramakrishnan, Pankajavalli; Dickson, Dennis W.; Davies, Peter

doi:10.1016/s0969-9961(03)00109-8

Cited by 81 publications

(51 citation statements)

References 40 publications

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“…In addition, Pin1 plays an important role in regulating the phosphorylationdephosphorylation of tau protein, APP, and other proteins such as cyclin dependent kinase-5, etc. In AD brain, Pin1 is found to be colocalized with phosphorylated tau and also shows an inverse relationship to the expression of tau in AD brains (196,316). Further, Pin1 was also identified by redox proteomics as oxidatively modified protein in AD hippocampus (65,363).…”

Section: Identification Of Carbonylated Proteins In Brainmentioning

confidence: 99%

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

157

142

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Several studies demonstrated that oxidative damage is a characteristic feature of many neurodegenerative diseases. The accumulation of oxidatively modified proteins may disrupt cellular functions by affecting protein expression, protein turnover, cell signaling, and induction of apoptosis and necrosis, suggesting that protein oxidation could have both physiological and pathological significance. For nearly two decades, our laboratory focused particular attention on studying oxidative damage of proteins and how their chemical modifications induced by reactive oxygen species/reactive nitrogen species correlate with pathology, biochemical alterations, and clinical presentations of Alzheimer's disease. This comprehensive article outlines basic knowledge of oxidative modification of proteins and lipids, followed by the principles of redox proteomics analysis, which also involve recent advances of mass spectrometry technology, and its application to selected age-related neurodegenerative diseases. Redox proteomics results obtained in different diseases and animal models thereof may provide new insights into the main mechanisms involved in the pathogenesis and progression of oxidativestress-related neurodegenerative disorders. Redox proteomics can be considered a multifaceted approach that has the potential to provide insights into the molecular mechanisms of a disease, to find disease markers, as well as to identify potential targets for drug therapy. Considering the importance of a better understanding of the cause/effect of protein dysfunction in the pathogenesis and progression of neurodegenerative disorders, this article provides an overview of the intrinsic power of the redox proteomics approach together with the most significant results obtained by our laboratory and others during almost 10 years of research on neurodegenerative disorders since we initiated the field of redox proteomics. Antioxid. Redox Signal. 17, 1610-1655.

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Section: Identification Of Carbonylated Proteins In Brainmentioning

confidence: 99%

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

157

142

View full text Add to dashboard Cite

show abstract

“…PIN1 is colocalized with phosphorylated tau and also shows an inverse relationship to the expression of tau in AD brain. Studies suggest that PIN1 can reduce the production of hyperphosphorylated tau (Holzer et al, 2002;Kurt et al, 2003;Ramakrishnan et al, 2003). PIN1 was found to be oxidized in AD brain, causing structural modifications and thereby affecting the properties of its targeted proteins, such as tau.…”

Section: Oxidatively Modified Proteins In Ad Brain Tissuementioning

confidence: 99%

Redox Proteomics: A New Approach to Investigate Oxidative Stress in Alzheimer's Disease

2006

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“…Microtubule breakdown induced by ischemia may impair trafficking, leading to cytoplasmic accumulation of HSP70 and peptidyl-prolyl cis/trans isomerases (PPIases) into large abnormal protein aggregates (Ramakrishnan et al, 2003;Liu et al, 2005a). Consistent with these data, PF preconditioning down-regulated the protein expression of HSP70 and PPIase.…”

Section: Preconditioning Induced By Pf 173mentioning

confidence: 58%

Involvement of Multitargets in Paeoniflorin-Induced Preconditioning

Chen¹,

Liang²,

Cai³

et al. 2006

J Pharmacol Exp Ther

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Paeoniflorin (PF) is the principal component of Paeoniae radix prescribed in traditional Chinese medicine. The delayed neuroprotection induced by PF preconditioning and its underlying mechanisms were investigated in rat middle cerebral artery occlusion (MCAO) and reperfusion model. At a dosage of 20 or 40 mg/kg, PF preconditioning 48 h before MCAO followed by 24-h reperfusion significantly reduced the mortality and infarct volume and reversed the neurological deficits caused by ischemia. Likewise, the ameliorative effects on mortality, infarct size, and neurological impairment induced by MCAO emerged as well when PF was administered 24 h, 48 h, or 5 days before MCAO at the dose of 20 mg/kg. Furthermore, comparative proteomics analysis was adopted to identify the differentially expressed proteins induced by PF preconditioning itself. The relative levels of 42 proteins were altered after PF preconditioning, among which 20 were elevated and 22 reduced. In summary, A 1 receptor-regulator of G protein signaling-K ATP signaling, arachidonic acid cascade, nitric oxide system, markers of neuronal damage, mitochondrial damage-related molecules, and the mitogen-activated protein kinase and nuclear factor-B pathway are associated with the mechanisms of PF preconditioning.Ischemic stroke is the second leading cause of death in China, leaving survivors burdened with severe disabilities. Deleterious infarctions of the middle cerebral artery (MCA) are at risk of developing massive edema because of the necrosis of cells located in the primary zone (Borlongan et al., 2005). The most effective drug, tissue plasminogen activator, the only Food and Drug Administration-approved thrombolytic drug used in ischemia, is widely employed in clinic. However, it has a very narrow therapeutic time window of 3 h, and only 1 to 3% of ischemic stroke patients have been benefited (Pulsinelli et al., 1997). Therefore, the current focus of stroke research requires investigation of novel neuroprotective agents and strategies, which could prolong the therapeutic window.Paeoniflorn (PF), the principal component of Paeoniae radix ("Shaoyao" in Chinese), has been widely investigated as antioxidant, cognitive enhancer, and endothelium-dependent vasodilator Ryu et al., 2001;Tabata et al., 2001). Recently, our laboratory found that PF could produce a dose-dependent decrease in both neurological impairment and infarct volume in acute transient cerebral ischemia through activating adenosine A 1 receptor in a manner different from its classic agonists (Liang et al., 2005;Liu et al., 2005b).Ischemic preconditioning (IPC) is an endogenous mechanism by which brief episodes of a sublethal insult induce a robust protection against the deleterious effects of subsequent, prolonged lethal ischemia. There are two kinds of protection: "classic IPC" and "delayed IPC." Various drugs ABBREVIATIONS: MCA, middle cerebral artery; PF, paeoniflorn; IPC, ischemic preconditioning; PPC, pharmacological preconditioning; DPCPX, 8-cyclopentyl-1,3-dipropylxanthine; TTC, 2,3,...

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Pin1 colocalization with phosphorylated tau in Alzheimer's disease and other tauopathies

Cited by 81 publications

References 40 publications

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Redox Proteomics: A New Approach to Investigate Oxidative Stress in Alzheimer's Disease

Involvement of Multitargets in Paeoniflorin-Induced Preconditioning

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