p(HBP:"APOE e4")
ApoE-epsilon4, but not ApoE-epsilon3, disrupts carbachol-stimulated phosphoinositol (PI) hydrolysis and so does Abeta and Abeta/ApoE-epsilon4 complexes in SH-SY5Y cells (Cedazo- Mínguez and Cowburn, 2001). The effect of Abeta and its ApoE complex on PI hydrolysis were blocked by estrogen, and this disruption was itself blocked by wortmannin, suggesting that PI3K mediates estrogen’s effect on PI hydrolysis. PubMed:19293145
The strongest identified genetic risk factor for LOAD is the apolipoprotein E (APOE) ε4 allele (APOE*ε4), PubMed:26195256
Our results indicated a significant down-regulation of PPP2R5E gene expression and reduction in PP2A activity by ApoE4 compared with ApoE3. This may also explain an elevated Tau phosphorylation in AD human brains that featured at least one ApoE4 allele. PubMed:28720530
ApoE-epsilon4, but not ApoE-epsilon3, disrupts carbachol-stimulated phosphoinositol (PI) hydrolysis and so does Abeta and Abeta/ApoE-epsilon4 complexes in SH-SY5Y cells (Cedazo- Mínguez and Cowburn, 2001). The effect of Abeta and its ApoE complex on PI hydrolysis were blocked by estrogen, and this disruption was itself blocked by wortmannin, suggesting that PI3K mediates estrogen’s effect on PI hydrolysis. PubMed:19293145
The strongest identified genetic risk factor for LOAD is the apolipoprotein E (APOE) ε4 allele (APOE*ε4), PubMed:26195256
Third, ApoE4 is also associated with lower antioxidant activity than other ApoE isoforms,154,155 and it mediates BBB breakdown through a proinflammatory pathway involving cyclophilin A in pericytes. PubMed:26195256
The pres- ence of ApoE4 is associated with reduced perivascular drainage of Aβ,161 which in turn is linked to deposition of immune complexes. PubMed:26195256
The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442
The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442
The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442
The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442
The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442
The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442
Our results indicated a significant down-regulation of PPP2R5E gene expression and reduction in PP2A activity by ApoE4 compared with ApoE3. This may also explain an elevated Tau phosphorylation in AD human brains that featured at least one ApoE4 allele. PubMed:28720530
Our results indicated a significant down-regulation of PPP2R5E gene expression and reduction in PP2A activity by ApoE4 compared with ApoE3. This may also explain an elevated Tau phosphorylation in AD human brains that featured at least one ApoE4 allele. PubMed:28720530
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.