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In-Edges 9

a(CHEBI:"GW 3965") directlyIncreases act(p(HGNC:NR1H3)) 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 3965") increases act(p(HGNC:NR1H3)) View Subject | View Object

Similarly, stimulation of microglia with the LXR agonist, GW3965, acts simultaneously to suppress inflammation and promote fibrillar Ab stimulated phagocytosis [47]. PubMed:21718217

a(CHEBI:cholesterol) increases act(p(HGNC:NR1H3)) View Subject | View Object

LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217

a(CHEBI:oxysterol) increases act(p(HGNC:NR1H3)) View Subject | View Object

LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217

a(CHEBI:oxysterol) increases act(p(HGNC:NR1H3)) View Subject | View Object

LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217

bp(GO:"cholesterol homeostasis") association p(HGNC:NR1H3) View Subject | View Object

LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217

bp(GO:"negative regulation of inflammatory response") association p(HGNC:NR1H3) View Subject | View Object

LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217

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

Additionally, PPAR-g can also induce the expression of LXRa creating a metabolically linked cycle. PubMed:21718217

Out-Edges 12

act(p(HGNC:NR1H3)) increases path(MESH:"Alzheimer Disease") View Subject | View Object

In the past decade, drugs targeting the NRs, peroxisome proliferator-activated receptor g (PPARg) and liver X receptor (LXR) have shown to ameliorate pathogenesis in animal models of AD. PubMed:21718217

act(p(HGNC:NR1H3)) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Recently, they have been shown to promote the degradation of the Ab peptides in the brain by activating genes responsible for reverse cholesterol transport [13]. PubMed:21718217

act(p(HGNC:NR1H3)) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

LXR activation increased the ApoE particle size of all human ApoE isoforms, suggesting that activation of this pathways may enhance Ab clearance regardless of the ApoE allele expressed [13]. PubMed:21718217

act(p(HGNC:NR1H3)) increases bp(GO:"reverse cholesterol transport") View Subject | View Object

Recently, they have been shown to promote the degradation of the Ab peptides in the brain by activating genes responsible for reverse cholesterol transport [13]. PubMed:21718217

act(p(HGNC:NR1H3)) decreases bp(GO:"microglial cell activation involved in immune response") View Subject | View Object

Activation of these receptors has been shown to suppress microglial-mediated inflammatory responses both in vitro and in vivo. PubMed:21718217

p(HGNC:NR1H3) association bp(GO:"cholesterol homeostasis") View Subject | View Object

LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217

p(HGNC:NR1H3) association bp(GO:"negative regulation of inflammatory response") View Subject | View Object

LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217

p(HGNC:NR1H3) increases p(HGNC:APOE) 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

act(p(HGNC:NR1H3)) increases act(p(HGNC:APOE)) View Subject | View Object

LXR activation increased the ApoE particle size of all human ApoE isoforms, suggesting that activation of this pathways may enhance Ab clearance regardless of the ApoE allele expressed [13]. 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

act(p(HGNC:NR1H3)) increases bp(GO:memory) View Subject | View Object

A different result was reported by Vanmierlo et al. who found that LXR agonist treatment resulted in restoration of memory, but did not find a change in plaque burden [48]. PubMed:21718217

act(p(HGNC:NR1H3)) decreases bp(GO:"microglial cell activation") View Subject | View Object

Indeed, treatment of AD mouse models with LXR or PPAR agonists has resulted in the suppression of microglial activation [44,45,47,59,63]. 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.