Publications by authors named "Moo-Rung Loo"

4 Publications

  • Page 1 of 1

Dream Lucidity and the Attentional Network Task.

Front Psychol 2021 28;12:586808. Epub 2021 Jan 28.

Institute of Cognitive Neuroscience, National Central University, Taoyuan, Taiwan.

This study investigated the relationship between dream lucidity, i.e., a dreamer's insight to the ongoing dream, and attention by considering lucidity as a trait. We examined the ways in which lucidity correlates with the orienting, alerting, and conflict components of the attentional network. A total of 77 participants rated the lucidity of their dreams over 7 consecutive days with the LuCiD scale and then completed the attentional network task (ANT). A negative correlation between trait lucidity and the conflict score of the ANT was found for 49 participants whose responses were faster when an alerting signal was presented. This result suggested that, with a prerequisite that the presence of cues facilitates subsequent information processing, the greater a person's trait lucidity, the more efficiently he or she is capable of resolving conflicts.
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http://dx.doi.org/10.3389/fpsyg.2021.586808DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7876060PMC
January 2021

Valproic acid enhances Oct4 promoter activity through PI3K/Akt/mTOR pathway activated nuclear receptors.

Mol Cell Endocrinol 2014 Mar 19;383(1-2):147-58. Epub 2013 Dec 19.

Department of Life Sciences, National Central University, Jhongli 32001, Taiwan. Electronic address:

Valproic acid (VPA) has been shown to increase the reprogramming efficiency of induced pluripotent stem cells (iPSC) from somatic cells, but the mechanism by which VPA enhances iPSC induction has not been defined. Here we demonstrated that VPA directly activated Oct4 promoter activity through activation of the PI3K/Akt/mTOR signaling pathway that targeted the proximal hormone response element (HRE, -41∼-22) in this promoter. The activating effect of VPA is highly specific as similar compounds or constitutional isomers failed to instigate Oct4 promoter activity. We further demonstrated that the upstream 2 half-sites in this HRE were essential to the activating effect of VPA and they were targeted by a subset of nuclear receptors, such as COUP-TFII and TR2. These findings show the first time that NRs are implicated in the VPA stimulated expression of stem cell-specific factors and should invite more investigation on the cooperation between VPA and NRs on iPSC induction.
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http://dx.doi.org/10.1016/j.mce.2013.12.008DOI Listing
March 2014

MicroRNA-3906 regulates fast muscle differentiation through modulating the target gene homer-1b in zebrafish embryos.

PLoS One 2013 31;8(7):e70187. Epub 2013 Jul 31.

Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan.

A microRNA, termed miR-In300 or miR-3906, suppresses the transcription of myf5 through silencing dickkopf-related protein 3 (dkk3r/dkk3a) during early development when myf5 is highly transcribed, but not at late stages when myf5 transcription is reduced. Moreover, after 24 hpf, when muscle cells are starting to differentiate, Dkk3a could not be detected in muscle tissue at 20 hpf. To explain these reversals, we collected embryos at 32 hpf, performed assays, and identified homer-1b, which regulates calcium release from sarcoplasmic reticulum, as the target gene of miR-3906. We further found that either miR-3906 knockdown or homer-1b overexpression increased expressions of fmhc4 and atp2a1 of calcium-dependent fast muscle fibrils, but not slow muscle fibrils, and caused a severe disruption of sarcomeric actin and Z-disc structure. Additionally, compared to control embryos, the intracellular calcium concentration ([Ca(2+)]i) of these treated embryos was increased as high as 83.9-97.3% in fast muscle. In contrast, either miR-3906 overexpression or homer-1b knockdown caused decreases of [Ca(2+)]i and, correspondingly, defective phenotypes in fast muscle. These defects could be rescued by inducing homer-1b expression at later stage. These results indicate that miR-3906 controls [Ca(2+)]i homeostasis in fast muscle through fine tuning homer-1b expression during differentiation to maintain normal muscle development.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0070187PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3729524PMC
April 2014

Valproic acid enhances Oct4 promoter activity in myogenic cells.

J Cell Biochem 2010 Jul;110(4):995-1004

Department of Life Sciences, National Central University, Jhongli 32054, Taiwan, ROC.

Induced pluripotent stem (iPS) cells are reprogrammed from somatic cells through ectopic expression of stem cell-specific transcription factors, including Oct4, Nanog, Sox2, Lin28, Klf4, and c-Myc. Although iPS cells are similar to embryonic stem (ES) cells in their pluripotency, their inherited defects, such as insertion mutagenesis, employment of oncogenes, and low efficiency, associated with the reprogramming procedure have hindered their clinical application. A study has shown that valproic acid (VPA) treatment can significantly enhance the reprogramming efficiency and avoid the usage of oncogenes. To understand how VPA can enhance pluripotency, we stably transfected an Oct4 promoter driven luciferase reporter (Oct4-1.9k-Luc) into P19 embryonic carcinoma (EC) cells and C2C12 myoblasts and examined their response to VPA. We found that VPA could both activate Oct4 promoter and rescue its inhibition by retinoic acid (RA). In C2C12 myoblasts, VPA treatment also enhanced endogenous Oct4 expression but repressed that of MyoD. Furthermore, both RARalpha over-expression and mutation of a proximal hormone response element (HRE) blocked the activation effect of VPA on Oct4 promoter, implying that VPA may exert its activation effect through factors targeting this HRE. Taken together, these observations identify a molecular mechanism by which VPA directly regulate Oct4 expression to ensure the acquirement and maintenance of pluripotency.
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http://dx.doi.org/10.1002/jcb.22613DOI Listing
July 2010