Journal Article (Review Article)

DZNE-2020-07430

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Biochemistry and cell biology of tau protein in neurofibrillary degeneration.

Mandelkow, E. M. (First author)DZNE* ; Mandelkow, E. (Last author)DZNE*

2012
Cold Spring Harbor Laboratory Press Cold Spring Harbor, NY

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Please use a persistent id in citations: doi:10.1101/cshperspect.a006247

Abstract: Tau represents the subunit protein of one of the major hallmarks of Alzheimer disease (AD), the neurofibrillary tangles, and is therefore of major interest as an indicator of disease mechanisms. Many of the unusual properties of Tau can be explained by its nature as a natively unfolded protein. Examples are the large number of structural conformations and biochemical modifications (phosphorylation, proteolysis, glycosylation, and others), the multitude of interaction partners (mainly microtubules, but also other cytoskeletal proteins, kinases, and phosphatases, motor proteins, chaperones, and membrane proteins). The pathological aggregation of Tau is counterintuitive, given its high solubility, but can be rationalized by short hydrophobic motifs forming β structures. The aggregation of Tau is toxic in cell and animal models, but can be reversed by suppressing expression or by aggregation inhibitors. This review summarizes some of the structural, biochemical, and cell biological properties of Tau and Tau fibers. Further aspects of Tau as a diagnostic marker and therapeutic target, its involvement in other Tau-based diseases, and its histopathology are covered by other chapters in this volume.

Keyword(s): Alzheimer Disease: metabolism (MeSH) ; Alzheimer Disease: pathology (MeSH) ; Animals (MeSH) ; Humans (MeSH) ; Microtubules (MeSH) ; Nerve Degeneration: metabolism (MeSH) ; Neurofibrillary Tangles (MeSH) ; Neurons: metabolism (MeSH) ; tau Proteins: chemistry (MeSH) ; tau Proteins: genetics (MeSH) ; tau Proteins: metabolism (MeSH) ; tau Proteins: ultrastructure (MeSH) ; tau Proteins

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Contributing Institute(s):

1. Cell and Animal Models of Neurodegeneration (AG Mandelkow 2)
2. Structural Principles of Neurodegeneration (AG Mandelkow 1)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2012

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Database coverage:
; BIOSIS Previews ; BIOSIS Reviews Reports And Meetings ; Clarivate Analytics Master Journal List ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; PubMed Central ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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