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Nuclear Functions of TOR: Impact on Transcription and the Epigenome

Authors
  • Laribee, R. Nicholas1
  • Weisman, Ronit2
  • 1 Department of Pathology and Laboratory Medicine, College of Medicine and Center for Cancer Research, University of Tennessee Health Science Center, 19 South Manassas, Cancer Research Building Rm 318, Memphis, TN 38163, USA
  • 2 Department of Natural and Life Sciences, The Open University of Israel, University Road 1, Ra’anana 4353701, Israel
Type
Published Article
Journal
Genes
Publisher
MDPI AG
Publication Date
Jun 10, 2020
Volume
11
Issue
6
Identifiers
DOI: 10.3390/genes11060641
PMID: 32532005
PMCID: PMC7349558
Source
PubMed Central
Keywords
License
Green

Abstract

The target of rapamycin (TOR) protein kinase is at the core of growth factor- and nutrient-dependent signaling pathways that are well-known for their regulation of metabolism, growth, and proliferation. However, TOR is also involved in the regulation of gene expression, genomic and epigenomic stability. TOR affects nuclear functions indirectly through its activity in the cytoplasm, but also directly through active nuclear TOR pools. The mechanisms by which TOR regulates its nuclear functions are less well-understood compared with its cytoplasmic activities. TOR is an important pharmacological target for several diseases, including cancer, metabolic and neurological disorders. Thus, studies of the nuclear functions of TOR are important for our understanding of basic biological processes, as well as for clinical implications.

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