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Article

c-jun N-terminal kinase hyperphosphorylates R406W tau at the PHF-1 site during mitosis.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology - 1 Apr 2006

Tatebayashi Yoshitaka, Planel Emmanuel, Chui De-Hua, Sato Shinji, Miyasaka Tomohiro, Sahara Naruhiko, Murayama Miyuki, Kikuchi Naomi, Yoshioka Katsuji, Rivka Ravid, Takashima Akihiko

Abstract excerpt

Tauopathies such as Alzheimer disease (AD) probably involve a type of phosphorylation imbalance causing the accumulation of abnormally hyperphosphorylated tau in neurons and/or glias. Investigation of R406W tau mutation may provide insight into such abnormal tau hyperphosphorylation, since this mutation causes AD-like dementia and tauopathy in humans and because it has the unique ability to reduce tau...

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PMID: 16478768
DOI: 10.1096/fj.05-4362fje

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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