Cited by 48Alzheimer's disease research and treatmentsProtein Kinase Regulation and GTPase SignalingDementia and Cognitive Impairment Research

Stimulation of MAP kinase by v‐raf transformation of fibroblasts fails to induce hyperphosphorylation of transfected tau

Latimer, Donna A., Gallo, Jean-Marc, Lovestone, Simon, Miller, Christopher C.J., Hugh Reynolds, C., Marquardt, Betina, Stabel, Silvia, Woodgett, James R. +1 more·1995·FEBS Letters

Abstract

A proportion of the microtubule‐associated protein, tau, is in an elevated state of phosphorylation in foetal and adult brain whereas all of the tau in paired helical filaments, which are characteristic of Alzheimer's disease is hyperphosphorylated; it is important therefore to elucidate the mechanisms that regulate tau phosphorylation. Here we describe results that show that although MAP kinase can hyperphosphorylate tau in vitro, activation of MAP kinase in transformed fibroblasts does not result in hyperphosphorylation of transfected tau, whereas glycogen synthase kinase‐3β (GSK‐3β) when co‐transfected with tau does result in tau hyperphosphorylation. The findings imply that GSK‐3β may be a stronger candidate than MAP kinase for inducing tau hyperphosphorylation in vivo.

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Crossref · 10.1016/0014-5793(95)00434-b

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  • GSK3β can orchestrate pathological tau phosphorylation at over two-dozen disease-associated sites.

    “The GSK3β can orchestrate pathological tau-phosphorylation at over two-dozen disease-associated sites [181–184].”

    From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [182]

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Authors
Latimer, D. A., Gallo, J.-M., Lovestone, S., Miller, C. C. J., Hugh Reynolds, C., Marquardt, B., Stabel, S., Woodgett, J. R., & Anderton, B. H.
Affiliations
  • Max Planck Society (DE)
  • Princess Margaret Cancer Centre (CA)
Venue
FEBS Letters
Publisher
Wiley
Published
1995-05-22
Volume
365
Issue
1
Pages
42-46
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
OpenAlex
W2029844247
Cited by
48
References
44
Citations by year
2025: 1 · 2023: 1 · 2019: 1 · 2012: 1
FWCI
3.76
Type
journal article
Language
en
Open access
closed
Locations
  • FEBS Letters (publishedVersion)
  • PubMed (publishedVersion)
Funders
Wellcome Trust
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
tau hyperphosphorylation, mitogen-activated protein kinase, glycogen synthase kinase-3β, fibroblasts, Alzheimer's disease, paired helical filaments, microtubule-associated proteins
MeSH terms
Animals, Enzyme Activation, Phosphorylation, Transformation, Genetic, Blotting, Western, Retroviridae Proteins, Oncogenic, 3T3 Cells, tau Proteins, Calcium-Calmodulin-Dependent Protein Kinases, Mitogen-Activated Protein Kinases, Oncogene Proteins v-raf, Glycogen Synthase Kinases, Glycogen Synthase Kinase 3, Mitogen-Activated Protein Kinase 3, Mice

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