ARL4C mRNA is translated

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R-HSA-9618405
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Reaction [omitted]
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Homo sapiens
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The ADP-ribosylation factor-like 4C (ARL4C or ARL7) mRNA is translated to yield ARL4C protein. ARL4C localizes to both the cell surface membrane and nucleus; however, a GDP-restricted mutant (Arl4c T27N) is mainly distributed in the cytoplasm (Engel T et al. 2004; Heo WD et al. 2006). Further, mutant constructs showed that effective plasma membrane targeting of ARL4C required an N-terminal myristoyl motif as well as a flexible C-terminal polybasic tail, which suggests that the two ends of the protein synergistically support cell surface targeting (Heo WD et al. 2006).

Cholesterol-loading or treatment with the synthetic agonists of liver X-receptors alpha (LXRα, NR1H3) and beta (LXRβ, NR1H2), such as T0901317 or GW3965, significantly induced the expression of ARL4C in murine RAW 264.7 and human THP1 macrophage cell lines (Hong C et al. 2011; Engel T et al. 2004; Sun D et al. 2012). Similar regulation of ARL4C mRNA expression was observed in human peripheral blood-derived monocytes (Hong C et al. 2011). NR1H2 or NR1H3 stimulation ARL4C has been shown to transport cholesterol to the membrane for the ATP-binding cassette transporter A1 (ABCA1)-associated cholesterol removal (Engel T et al. 2004). Overexpression of ARL4C in HeLa cells has been shown to enhance APOA1-mediated cholesterol efflux (Engel T et al. 2004). MicroRNA miR-26 represses NR1H2,3-dependent cholesterol efflux by targeting ARL4C mRNA (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
21187453 Constitutive activation of LXR in macrophages regulates metabolic and inflammatory gene expression: identification of ARL7 as a direct target

Hong, C, Walczak, R, Dhamko, H, Bradley, MN, Marathe, C, Boyadjian, R, Salazar, JV, Tontonoz, P

J. Lipid Res. 2011
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