Aphidicolin glycinate inhibits human neuroblastoma cell growth in vivo.

Author(s):  
J Cinatl ◽  
R Kotchetkov ◽  
P H Driever ◽  
S Bertels ◽  
K Siems ◽  
...  
1993 ◽  
Vol 48 (1-2) ◽  
pp. 217-224 ◽  
Author(s):  
Mihir A. Meghani ◽  
Donna M. Martin ◽  
J.Robinson Singleton ◽  
Eva L. Feldman

2013 ◽  
Vol 29 (5) ◽  
pp. 1714-1720 ◽  
Author(s):  
M. WAHEED ROOMI ◽  
TATIANA KALINOVSKY ◽  
NUSRATH W. ROOMI ◽  
ALEKSANDRA NIEDZWIECKI ◽  
MATTHIAS RATH

2017 ◽  
Vol 105 (8) ◽  
pp. 2129-2138 ◽  
Author(s):  
A. Ajetunmobi ◽  
D. McAllister ◽  
N. Jain ◽  
O. Brazil ◽  
A. Corvin ◽  
...  

2013 ◽  
Vol 30 (3) ◽  
pp. 675-679
Author(s):  
Mahshid Nikpour Nezhati ◽  
Gholam Hossein Riazi ◽  
Homayon Ahmad Panahi ◽  
Elham Moniri ◽  
Nasir Ahmad Rajabi ◽  
...  

2019 ◽  
Author(s):  
Mercedes Arnés ◽  
Ninovska Romero ◽  
Sergio Casas-Tintó ◽  
Ángel Acebes ◽  
Alberto Ferrús

AbstractAlzheimer’s disease is, to a large extent, a disease of the synapse triggered by the unbalanced amyloidogenic cleavage of the amyloid precursor protein APP. Excess of Aβ42 peptide in particular is considered a hallmark of the disease. Here we drive the expression of the human Aβ42 peptide to assay the neuroprotective effects of PI3K in adult Drosophila melanogaster. We show that the neuronal expression of the human peptide elicits progressive toxicity in the adult. The pathological traits include reduced axonal transport, synapse loss, defective climbing ability and olfactory perception, as well as life-span reduction. The Aβ42-dependent synapse decay does not involve transcriptional changes in the core synaptic protein encoding genes: bruchpilot, liprin and synaptobrevin. All toxicity features, however, are suppressed by the co-expression of PI3K. Moreover, PI3K activation induces a significant increase of 6E10 and Thioflavin-positive amyloid deposits. Mechanistically, we suggest that Aβ42-Ser26 could be a candidate residue for direct or indirect phosphorylation by PI3K. Finally, along with these in vivo experiments we further analyze Aβ42 toxicity and its suppression by PI3K activation in in vitro assays with SH-SY5Y human neuroblastoma cell cultures, where Aβ42 aggregation into large insoluble deposits is reproduced. Taken together, these results uncover a potential novel pharmacological strategy against this disease with PI3K activation as a target.


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