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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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Related Experiment Video

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Long noncoding RNA MEG3: an active player in fibrosis.

Xiaoying Jiang1

  • 1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 Yanta West Road, Xi'an, Shaanxi, 710061, China. jiangxy@mail.xjtu.edu.cn.

Pharmacological Reports : PR
|October 7, 2024
PubMed
Summary

The long noncoding RNA maternally expressed gene 3 (MEG3) plays a key role in fibrosis development. Modulating MEG3 levels can help treat fibrosis by targeting key signaling pathways.

Keywords:
FibrosisLong noncoding RNAsMEG3Potential target

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Pathology

Background:

  • Fibrosis involves excessive extracellular matrix accumulation, leading to tissue damage and organ dysfunction.
  • Long noncoding RNAs (lncRNAs) are non-protein-coding transcripts longer than 200 nucleotides.
  • The lncRNA maternally expressed gene 3 (MEG3) is increasingly recognized for its involvement in fibrotic processes across various tissues.

Purpose of the Study:

  • To review and summarize the current understanding of lncRNA MEG3's role in fibrosis.
  • To elucidate the molecular mechanisms by which MEG3 influences fibrotic development.
  • To highlight the therapeutic potential of targeting MEG3 in fibrotic diseases.

Main Methods:

  • Literature review of studies investigating lncRNA MEG3 in fibrosis.
  • Analysis of MEG3's regulatory functions, including protein targets and miRNA sponging.
  • Examination of signaling pathways implicated in MEG3-mediated fibrosis.

Main Results:

  • MEG3 is dysregulated in multiple fibrotic conditions.
  • MEG3 regulates fibrosis through interactions with key signaling pathways such as NF-κB, PI3K/AKT, JAK2/STAT3, Wnt/β-catenin, ERK/p38, and Hh.
  • Interfering with MEG3 levels has shown a ameliorating effect on fibrosis.

Conclusions:

  • lncRNA MEG3 is a critical regulator in the pathogenesis of fibrosis.
  • MEG3 influences fibrosis by modulating diverse cellular signaling pathways.
  • Targeting MEG3 presents a promising therapeutic strategy for treating fibrotic diseases.