Literature DB >> 29248739

Maf1 phenotypes and cell physiology.

Ian M Willis1.   

Abstract

As a master regulator of transcription by RNA polymerase (Pol) III, Maf1 represses the synthesis of highly abundant non-coding RNAs as anabolic signals dissipate, as the quality or quantity of nutrients decreases, and under a wide range of cellular and environmental stress conditions. Thus, Maf1 responds to changes in cell physiology to conserve metabolic energy and to help maintain appropriate levels of tRNAs and other essential non-coding RNAs. Studies in different model organisms and cell-based systems show that perturbations of Maf1 can also impact cell physiology and metabolism. These effects are mediated by changes in Pol III transcription and/or by effects of Maf1 on the expression of select Pol II-transcribed genes. Maf1 phenotypes can vary between different systems and are sometimes conflicting as in comparisons between Maf1 KO mice and cultured mammalian cells. These studies are reviewed in an effort to better appreciate the relationship between Maf1 function and cell physiology. This article is part of a Special Issue entitled: SI: Regulation of tRNA synthesis and modification in physiological conditions and disease edited by Dr. Boguta Magdalena.
Copyright © 2017 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Maf1; RNA polymerase III; cancer; futile cycle; metabolism; tumor suppressor

Mesh:

Substances:

Year:  2017        PMID: 29248739      PMCID: PMC5882558          DOI: 10.1016/j.bbagrm.2017.11.009

Source DB:  PubMed          Journal:  Biochim Biophys Acta Gene Regul Mech        ISSN: 1874-9399            Impact factor:   4.490


  65 in total

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  8 in total

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2.  Metabolic programming a lean phenotype by deregulation of RNA polymerase III.

Authors:  Ian M Willis; Robyn D Moir; Nouria Hernandez
Journal:  Proc Natl Acad Sci U S A       Date:  2018-11-14       Impact factor: 11.205

Review 3.  RNA Polymerases I and III in development and disease.

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4.  A cancer-associated RNA polymerase III identity drives robust transcription and expression of snaR-A noncoding RNA.

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5.  RNA polymerase III subunits C37/53 modulate rU:dA hybrid 3' end dynamics during transcription termination.

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6.  Maf1 ameliorates cardiac hypertrophy by inhibiting RNA polymerase III through ERK1/2.

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Journal:  Theranostics       Date:  2019-09-25       Impact factor: 11.556

7.  Maf1 suppression of ATF5-dependent mitochondrial unfolded protein response contributes to rapamycin-induced radio-sensitivity in lung cancer cell line A549.

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Review 8.  Brain delivering RNA-based therapeutic strategies by targeting mTOR pathway for axon regeneration after central nervous system injury.

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  8 in total

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