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Entity

Name
all-trans-retinoic acid
Namespace
chebi
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/chebi-names.belns

Appears in Networks 2

In-Edges 0

Out-Edges 10

a(CHEBI:"all-trans-retinoic acid") increases act(p(FPLX:RXR)) View Subject | View Object

ATRA not only activates RXR but also activates the retinoic acid receptor. PubMed:21718217

a(CHEBI:"all-trans-retinoic acid") increases act(p(FPLX:RAR)) View Subject | View Object

ATRA not only activates RXR but also activates the retinoic acid receptor. PubMed:21718217

a(CHEBI:"all-trans-retinoic acid") decreases a(HBP:HBP00018) View Subject | View Object

Treatment of 5-month-old APP/PS1 mice for 8 weeks with ATRA (20 mg/kg/day) resulted in significant decreases in Ab deposition and tau phosphorylation in these mice. Additionally, it attenuated memory deficits seen in the Morris water maze [77]. PubMed:21718217

a(CHEBI:"all-trans-retinoic acid") decreases p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

Treatment of 5-month-old APP/PS1 mice for 8 weeks with ATRA (20 mg/kg/day) resulted in significant decreases in Ab deposition and tau phosphorylation in these mice. Additionally, it attenuated memory deficits seen in the Morris water maze [77]. PubMed:21718217

a(CHEBI:"all-trans-retinoic acid") increases bp(GO:memory) View Subject | View Object

Treatment of 5-month-old APP/PS1 mice for 8 weeks with ATRA (20 mg/kg/day) resulted in significant decreases in Ab deposition and tau phosphorylation in these mice. Additionally, it attenuated memory deficits seen in the Morris water maze [77]. PubMed:21718217

a(CHEBI:"all-trans-retinoic acid") decreases path(MESH:"Plaque, Amyloid") View Subject | View Object

ATRA prevents the accumulation of amyloid plaques and APP processing into Ab through downregulation of Cdk5 in APP/PS1 mice. These results suggested that the administration of ATRA inhibited activity of Cdk5 and GSK3b and attenuated the formation of p-tau aggregation, including p-CRMP2 and p-WAVE1 in the 33Tg mouse brain. PubMed:26400044

Appears in Networks:

a(CHEBI:"all-trans-retinoic acid") decreases a(HBP:"APP processing") View Subject | View Object

ATRA prevents the accumulation of amyloid plaques and APP processing into Ab through downregulation of Cdk5 in APP/PS1 mice. These results suggested that the administration of ATRA inhibited activity of Cdk5 and GSK3b and attenuated the formation of p-tau aggregation, including p-CRMP2 and p-WAVE1 in the 33Tg mouse brain. PubMed:26400044

Appears in Networks:

a(CHEBI:"all-trans-retinoic acid") decreases act(p(MGI:Cdk5), ma(kin)) View Subject | View Object

ATRA prevents the accumulation of amyloid plaques and APP processing into Ab through downregulation of Cdk5 in APP/PS1 mice. These results suggested that the administration of ATRA inhibited activity of Cdk5 and GSK3b and attenuated the formation of p-tau aggregation, including p-CRMP2 and p-WAVE1 in the 33Tg mouse brain. PubMed:26400044

Appears in Networks:

a(CHEBI:"all-trans-retinoic acid") decreases act(p(MGI:Gsk3b), ma(kin)) View Subject | View Object

ATRA prevents the accumulation of amyloid plaques and APP processing into Ab through downregulation of Cdk5 in APP/PS1 mice. These results suggested that the administration of ATRA inhibited activity of Cdk5 and GSK3b and attenuated the formation of p-tau aggregation, including p-CRMP2 and p-WAVE1 in the 33Tg mouse brain. PubMed:26400044

Appears in Networks:

a(CHEBI:"all-trans-retinoic acid") decreases complex(p(MGI:Dpysl2, pmod(Ph)), p(MGI:Mapt), p(MGI:Wasf1, pmod(Ph))) View Subject | View Object

ATRA prevents the accumulation of amyloid plaques and APP processing into Ab through downregulation of Cdk5 in APP/PS1 mice. These results suggested that the administration of ATRA inhibited activity of Cdk5 and GSK3b and attenuated the formation of p-tau aggregation, including p-CRMP2 and p-WAVE1 in the 33Tg mouse brain. PubMed:26400044

Appears in Networks:

About

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.