Title : Suppression of neuronal cholesterol biosynthesis impairs brain functions through insulin-like growth factor I-Akt signaling.

Pub. Date : 2021

PMID : 34671194






3 Functional Relationships(s)
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1 Treatment with U18666A reduced the cellular cholesterol level and blocked the anti-apoptotic function of IGF-1 by impairing the formation of caveolae and the localization of IGF-1 receptor in caveolae of the PC12 cells. 3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one insulin-like growth factor 1 Rattus norvegicus
2 Furthermore, the phosphorylation levels of IGF-1 receptor, insulin receptor substrate (IRS), Akt, and Bad in response to IGF-1 were all found to decrease in the U18666A-treated cells. 3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one insulin-like growth factor 1 Rattus norvegicus
3 Rats treated with U18666A via intracerebral injection also exhibited a significant decrease in the cholesterol level and impaired activities of IGF-1-related signaling proteins in the hippocampus region. 3-beta-(2-(diethylamino)ethoxy)androst-5-en-17-one insulin-like growth factor 1 Rattus norvegicus