2006
DOI: 10.1128/mcb.02393-05
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Abstract: Amyloid precursor protein (APP) has eight potential phosphorylation sites in its cytoplasmic domain.Recently, it has demonstrated that the constitutive phosphorylation of APP at T668 (APP695 isoform numbering) was observed specifically in the brain. Neuron-specific phosphorylation of APP at T668 is thought to be important for neuronal functions of APP, although its exact physiological significance remains to be clarified. In this study, we show that the phosphorylation of the APP intracellular domain (AICD) at… Show more

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Cited by 148 publications
(113 citation statements)
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“…It is of particular significance that APP can be phosphorylated on Thr-668 by cdk5 and glycogen-synthase kinase 3, two tau protein kinases that have been implicated in the neurofibrillary degeneration in AD (Stoothoff and Johnson, 2005). Notably, phosphorylation at Thr-668 has been linked to increased amyloidogenic processing of APP (Ando et al, 2001;Liu et al, 2003;Phiel et al, 2003;Vingtdeux et al, 2005;Chang et al, 2006;Pierrot et al, 2006). Accordingly, enhanced APP phosphorylation at the Thr-668 site correlated with increased A␤ production in our experiments.…”
Section: Discussionsupporting
confidence: 50%
“…It is of particular significance that APP can be phosphorylated on Thr-668 by cdk5 and glycogen-synthase kinase 3, two tau protein kinases that have been implicated in the neurofibrillary degeneration in AD (Stoothoff and Johnson, 2005). Notably, phosphorylation at Thr-668 has been linked to increased amyloidogenic processing of APP (Ando et al, 2001;Liu et al, 2003;Phiel et al, 2003;Vingtdeux et al, 2005;Chang et al, 2006;Pierrot et al, 2006). Accordingly, enhanced APP phosphorylation at the Thr-668 site correlated with increased A␤ production in our experiments.…”
Section: Discussionsupporting
confidence: 50%
“…NATURE COMMUNICATIONS | DOI: 10.1038/ncomms4330 ARTICLE the exact molecular mechanism of how APP-mediated regulation of miR-574-5p transcription is unclear, we speculate that APP may directly bind to the genomic regions surrounding miR-574-5p through intracellular C-terminal Domain (AICD) of APP, given that AICD can translocate to nucleus upon phosphorylation of APP and mediate some nuclear signalling events [26][27][28] . Next, what is the molecular target of miR-574-5p in regulating the proliferation and differentiation of NPCs?…”
Section: Discussionmentioning
confidence: 99%
“…Active JNK phophorylates AP1 transcription factors to regulate gene expression (i), and APP at T668 to enhance the amyloidogenic cleavage of APP (ii). CTF␤ generated by ␤-secretase is processed by ␥-secretase to produce a phosphorylated form of AICD, which can translocate to the nucleus (Chang et al, 2006), and more A␤, which further stimulates JNK activity. Sustained high-level JNK activity in the brain induces caspase activation (iii) causing synaptic dysfunction (D'Amelio et al, 2011) and/or neuronal death.…”
Section: Discussionmentioning
confidence: 99%