Upregulation of Thioredoxin-Interacting Protein in Brain of Amyloid-β Protein Precursor/Presenilin 1 Transgenic Mice and Amyloid-β Treated Neuronal Cells

2019 ◽  
Vol 72 (1) ◽  
pp. 139-150 ◽  
Author(s):  
Yiran Wang ◽  
Ying Wang ◽  
Veni Bharti ◽  
Hong Zhou ◽  
Vanessa Hoi ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Neuronal Cells ◽  
Amyloid Β ◽  
Presenilin 1 ◽  
Amyloid Β Protein ◽  
Interacting Protein ◽  
Protein Precursor ◽  
Thioredoxin Interacting Protein ◽  
Β Protein

scholarly journals Phosphorylation of KLC1 modifies interaction with JIP1 and abolishes the enhanced fast velocity of APP transport by kinesin-1

2017 ◽  
Vol 28 (26) ◽  
pp. 3857-3869 ◽  
Author(s):  
Kyoko Chiba ◽  
Ko-yi Chien ◽  
Yuriko Sobu ◽  
Saori Hata ◽  
Shun Kato ◽  
...  
Keyword(s):  
Coiled Coil ◽  
Amyloid Β ◽  
Tetratricopeptide Repeat ◽  
Amyloid Β Protein ◽  
The Novel ◽  
Anterograde Transport ◽  
Interacting Protein ◽  
Protein Precursor ◽  
Kinesin Light Chain ◽  
Β Protein

In neurons, amyloid β-protein precursor (APP) is transported by binding to kinesin-1, mediated by JNK-interacting protein 1b (JIP1b), which generates the enhanced fast velocity (EFV) and efficient high frequency (EHF) of APP anterograde transport. Previously, we showed that EFV requires conventional interaction between the JIP1b C-terminal region and the kinesin light chain 1 (KLC1) tetratricopeptide repeat, whereas EHF requires a novel interaction between the central region of JIP1b and the coiled-coil domain of KLC1. We found that phosphorylatable Thr466 of KLC1 regulates the conventional interaction with JIP1b. Substitution of Glu for Thr466 abolished this interaction and EFV, but did not impair the novel interaction responsible for EHF. Phosphorylation of KLC1 at Thr466 increased in aged brains, and JIP1 binding to kinesin-1 decreased, suggesting that APP transport is impaired by aging. We conclude that phosphorylation of KLC1 at Thr466 regulates the velocity of transport of APP by kinesin-1 by modulating its interaction with JIP1b.

Transcranial Laser Therapy Attenuates Amyloid-β Peptide Neuropathology in Amyloid-β Protein Precursor Transgenic Mice

2011 ◽  
Vol 23 (3) ◽  
pp. 521-535 ◽  
Author(s):  
Luis De Taboada ◽  
Jin Yu ◽  
Salim El-Amouri ◽  
Sebastiano Gattoni-Celli ◽  
Steve Richieri ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Laser Therapy ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Amyloid Β Protein ◽  
Protein Precursor ◽  
Β Protein

scholarly journals Dysregulation of Amyloid-β Protein Precursor, β-Secretase, Presenilin 1 and 2 Genes in the Rat Selectively Vulnerable CA1 Subfield of Hippocampus Following Transient Global Brain Ischemia

2015 ◽  
Vol 47 (4) ◽  
pp. 1047-1056 ◽  
Author(s):  
Janusz Kocki ◽  
Marzena Ułamek-Kozioł ◽  
Anna Bogucka-Kocka ◽  
Sławomir Januszewski ◽  
Mirosław Jabłoński ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Amyloid Β ◽  
Presenilin 1 ◽  
Amyloid Β Protein ◽  
Global Brain Ischemia ◽  
Protein Precursor ◽  
Β Protein ◽  
Global Brain

Impaired neurotransmitter systems by Aβ amyloidosis in APPsw transgenic mice overexpressing amyloid β protein precursor

2000 ◽  
Vol 292 (3) ◽  
pp. 155-158 ◽  
Author(s):  
Yasushi Tomidokoro ◽  
Yasuo Harigaya ◽  
Etsuro Matsubara ◽  
Masaki Ikeda ◽  
Takeshi Kawarabayashi ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Protein Precursor ◽  
Neurotransmitter Systems ◽  
Β Protein
Sign in / Sign up

Export Citation Format

Share Document