miR-26 binds to the 3'UTR of the ARL4C mRNA

Stable Identifier
R-HSA-9618392
Type
Reaction [binding]
Species
Homo sapiens
Compartment
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A 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).

Literature References
PubMed ID Title Journal Year
22673513 MiR-26 controls LXR-dependent cholesterol efflux by targeting ABCA1 and ARL7

Sun, D, Zhang, J, Xie, J, Wei, W, Chen, M, Zhao, X

FEBS Lett. 2012
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