Reactome: A Curated Pathway Database
THIS SITE IS USED FOR CURATION AND TESTING
IT IS NOT STABLE, IS LINKED TO AN INCOMPLETE DATA SET, AND IS NOT MONITORED FOR PERFORMANCE. WE STRONGLY RECOMMEND THE USE OF OUR PUBLIC SITE

Query author contributions in Reactome

Reactome depends on collaboration between our curation team and outside experts to assemble and peer-review its pathway modules. The integration of ORCID within Reactome enables us to meet a key challenge with authoring, curating and reviewing biological information by incentivizing and crediting the external experts that contribute their expertise and time to the Reactome curation process. More information is available at ORCID and Reactome.

If you have an ORCID ID that is not listed on this page, please forward this information to us and we will update your Reactome pathway records.

Name Email address

Details on Person A small non-coding RNA miR-26 was identified as a liver X re...

Class:IdSummation:9618404
_displayNameA small non-coding RNA miR-26 was identified as a liver X re...
_timestamp2019-08-14 04:23:51
created[InstanceEdit:9618398] Shamovsky, Veronica, 2018-09-06
literatureReference[LiteratureReference:9618471] MiR-26 controls LXR-dependent cholesterol efflux by targeting ABCA1 and ARL7
modified[InstanceEdit:9618472] Shamovsky, Veronica, 2018-09-06
[InstanceEdit:9618484] Shamovsky, Veronica, 2018-09-07
[InstanceEdit:9619446] Shamovsky, Veronica, 2018-09-17
[InstanceEdit:9634037] Shamovsky, Veronica, 2019-01-03
[InstanceEdit:9658354] Shamovsky, Veronica, 2019-08-13
[InstanceEdit:9658428] Shamovsky, Veronica, 2019-08-14
textA small non-coding RNA miR-26 was identified as a liver X receptor (LXR or NR1H2,3)-responsive miRNA that is downregulated in the presence of LXR agonist T0901317 (Sun D et al. 2012). miR-26 suppressed the translation of ADP-ribosylation factor-like 4C (ARL4C or ARL7) mRNA in NR1H2,3 (LXR)‐activated human (THP-1) and mouse (RAW264.7) macrophages. Bioinformatic tools for miRNA target prediction showed that the seed regions of miR‐26a and miR‐26b were complementary to the ARL4C 3′UTR (Sun D et al. 2012). The miR-26 binding sites in ARL4C 3′UTR were highly conserved among mammals (Sun D et al. 2012). Further, 3'UTR luciferase reporter assay using human embryonic kidney cells (HEK293T) showed that a miR-26 mimetic inhibits ARL4C 3′UTR luciferase reporter activity and this is absent with the mutant ARL4C 3′UTR firefly luciferase reporter (Sun D et al. 2012). Similar results were obtained for another NR1H2,3-regulated gene ATP-binding cassette transporter A1 (ABCA1). Moreover, miR‐26 was shown to suppress the NR1H2,3‐dependent cholesterol efflux in RAW264.7 cells by targeting ARL4C and ABCA1 (Sun D et al. 2012). This Reactome event describes the miR-26-regulated translation of ARL4C mRNA in responce to NR1H2,3 ligands. The annotation is based on the study with GW3965 and T0901317, the synthetic agonists of NR1H2,3 (Sun D et al. 2012).
(summation)[Reaction:9618392] miR-26 binds to the 3'UTR of the ARL4C mRNA [Homo sapiens]
[Change default viewing format]
No pathways have been reviewed or authored by A small non-coding RNA miR-26 was identified as a liver X re... (9618404)