Direct interaction of soluble human recombinant tau protein with Abeta 1-42 results in tau aggregation and hyperphosphorylation by tau protein kinase II. (Q40739303)

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scientific article published on March 2002

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English	Direct interaction of soluble human recombinant tau protein with Abeta 1-42 results in tau aggregation and hyperphosphorylation by tau protein kinase II.	scientific article published on March 2002

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9 December 2019

Direct interaction of soluble human recombinant tau protein with Abeta 1-42 results in tau aggregation and hyperphosphorylation by tau protein kinase II (English)

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9 December 2019

Jennifer A. Johnston

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9 December 2019

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Kenneth B Rank

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9 December 2019

Adele M Pauley

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9 December 2019

Keshab Bhattacharya

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9 December 2019

Zhigang Wang

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9 December 2019

David B Evans

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9 December 2019

Timothy J Fleck

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9 December 2019

Satish K Sharma

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9 December 2019

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1 March 2002

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9 December 2019

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9 December 2019

514

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9 December 2019

2-3

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9 December 2019

263-268

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9 December 2019

Alzheimer plaques and tangles: advances on both fronts

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Accumulation of abnormally phosphorylated tau precedes the formation of neurofibrillary tangles in Alzheimer's disease

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Tau protein and the neurofibrillary pathology of Alzheimer's disease

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A preparation of Alzheimer paired helical filaments that displays distinct tau proteins by polyacrylamide gel electrophoresis

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Structural stability of paired helical filaments requires microtubule-binding domains of Tau: A model for self-association

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A68: a major subunit of paired helical filaments and derivatized forms of normal Tau.

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Multiple isoforms of human microtubule-associated protein tau: sequences and localization in neurofibrillary tangles of Alzheimer's disease

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Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration

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21 January 2018

Tau phosphorylation at serine 396 and serine 404 by human recombinant tau protein kinase II inhibits tau's ability to promote microtubule assembly

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Carboxyl-terminal fragments of Alzheimer beta-amyloid precursor protein accumulate in restricted and unpredicted intracellular compartments in presenilin 1-deficient cells.

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Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

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Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

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21 January 2018

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