Racemic N1-Norphenserine and Its Enantiomers: Unpredicted Inhibition of Human Acetyl- and Butyrylcholinesterase and β-Amyloid Precursor Protein in vitro

Heterocycles ◽  
2003 ◽  
Vol 61 (1) ◽  
pp. 529 ◽  
Author(s):  
Nigel H. Greig ◽  
Qian-sheng Yu ◽  
Weiming Luo ◽  
Harold W. Holloway ◽  
Tada Utsuki ◽  
...  
Keyword(s):  
Amyloid Precursor Protein ◽  
Precursor Protein ◽  
Β Amyloid

Nerve growth factor does not influence the expression of β amyloid precursor protein mRNA in rat brain: in vivo and in vitro studies

1993 ◽  
Vol 620 (2) ◽  
pp. 292-296 ◽  
Author(s):  
Gianluigi Forloni ◽  
Roberto Del Bo ◽  
Nadia Angeretti ◽  
Simona Smiroldo ◽  
Nadia Gabellini ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Amyloid Precursor Protein ◽  
Rat Brain ◽  
Precursor Protein ◽  
In Vitro Studies ◽  
Nerve Growth ◽  
Β Amyloid

scholarly journals Suppression of β-Amyloid Precursor Protein Signaling into the Nucleus by Estrogens Mediated through Complex Formation between the Estrogen Receptor and Fe65

2006 ◽  
Vol 27 (4) ◽  
pp. 1321-1333 ◽  
Author(s):  
Junying Bao ◽  
Chuanhai Cao ◽  
Xiaohui Zhang ◽  
Feng Jiang ◽  
Santo V. Nicosia ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Amyloid Precursor Protein ◽  
Estrogen Receptor Alpha ◽  
Neuronal Degeneration ◽  
Adaptor Protein ◽  
Precursor Protein ◽  
Protein Signaling ◽  
Multimeric Complex ◽  
Β Amyloid

ABSTRACT The C-terminal fragment of the β-amyloid precursor protein produced after cleavage by γ-secretase, namely, APPct or AICD, has been shown to form a multimeric complex with the adaptor protein Fe65 and to regulate transcription through the recruitment of the histone acetyltransferase Tip60. The present study shows that 17β-estradiol inhibits the transcriptional and apoptotic activities of the APPct complex by a process involving the interaction of estrogen receptor alpha (ERα) with Fe65. ERα-Fe65 complexes were detected both in vitro and in the mouse brain, and recruitment of ERα to the promoter of an APPct target gene (KAI1) was demonstrated. Our studies reveal a novel mechanism of estrogen action, which may explain the well-known neuroprotective functions of estrogens as well as the complex role of this female hormone in the pathogenesis of neuronal degeneration diseases.

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