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Appears in Networks 1

In-Edges 7

a(CHEBI:"GW 3965") increases p(HGNC:ABCA1) View Subject | View Object

Importantly, this study utilized the LXR agonist, GW3965, to activate the LXRs and induce the expression of both ApoE and ABCA1. PubMed:21718217

a(CHEBI:"GW 501516") increases p(HGNC:ABCA1) View Subject | View Object

The PPAR-d agonist GW501516 induced expression of ABCA1 and apolipoprotein A1, a peripheral lipid transporter, in macrophages [71]. PubMed:21718217

a(CHEBI:Honokiol) increases p(HGNC:ABCA1) View Subject | View Object

More recently, a naturally occurring RXR agonist, honokiol, has been identified. This agonist is capable of activating RXR/LXR heterodimers and has been shown to induce the expression of ABCA1 and ApoE and should be tested in AD models [75,78]. PubMed:21718217

a(CHEBI:bexarotene) increases p(HGNC:ABCA1) View Subject | View Object

Bexarotene is a highly specific RXR agonist and is currently FDA approved with a favorable side effect profile. Studies in our laboratory have shown that treatment of APP/ PS1 animals with bexarotene for only 3 days results in a dramatic induction of ApoE and ABCA1 and the rapid reversal of AD-associated pathological hallmarks including reduction in amyloid deposition and deficits in behavior as well as neural networks. PubMed:21718217

act(p(FPLX:RXR)) increases p(HGNC:ABCA1) View Subject | View Object

RXR activation by numerous ligands has shown to increase levels of both ApoE and ABCA1 in vitro [74-76]. PubMed:21718217

p(HGNC:NR1H3) increases p(HGNC:ABCA1) View Subject | View Object

Numerous studies have shown that both PPAR-g and LXRs induce the expression of ApoE and ABCA1 and it is through the expression of these proteins that they exert their effects on amyloid pathology. PubMed:21718217

p(HGNC:PPARG) increases p(HGNC:ABCA1) View Subject | View Object

Numerous studies have shown that both PPAR-g and LXRs induce the expression of ApoE and ABCA1 and it is through the expression of these proteins that they exert their effects on amyloid pathology. PubMed:21718217

Out-Edges 2

p(HGNC:ABCA1) increases p(HGNC:APOE) View Subject | View Object

The loss of abca1 resulted in not only the reduction of ApoE levels but also a paradoxical increase in Ab deposition in the brain parenchyma of these animals owing to enhanced deposition of poorly lipidated ApoE in the brain [50-52]. PubMed:21718217

p(HGNC:ABCA1) decreases a(HBP:HBP00018) View Subject | View Object

The loss of abca1 resulted in not only the reduction of ApoE levels but also a paradoxical increase in Ab deposition in the brain parenchyma of these animals owing to enhanced deposition of poorly lipidated ApoE in the brain [50-52]. PubMed:21718217

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BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.