Tumor suppressor p53 and estrogen receptors in nuclear-mitochondrial communication.

Mitochondrion

Department of Pharmacology and Therapeutics, Center for Genetics and Pharmacology, Roswell Park Cancer Institute, Elm & Carlton Streets, Buffalo, NY 14263, United States. Electronic address:

Published: May 2014

AI Article Synopsis

  • Several gene regulators typically found in the nucleus are now being detected in mitochondria, sparking interest in mitochondrial roles in cell metabolism in both healthy and disease conditions.
  • Research highlights important interactions between nuclear and mitochondrial components (genomes, transcriptomes, and proteomes) that influence cell functions.
  • Tumor suppressor p53 and estrogen receptor (ER) have roles in both the nucleus and mitochondria, with p53 performing transcription-independent tasks in mitochondria, while the exact functions of mitochondrial ERs are still being investigated.

Article Abstract

Several gene transcription regulators considered solely localized within the nuclear compartment are being reported to be present in the mitochondria as well. There is growing interest in the role of mitochondria in regulating cellular metabolism in normal and disease states. Various findings demonstrate the importance of crosstalk between nuclear and mitochondrial genomes, transcriptomes, and proteomes in regulating cellular functions. Both tumor suppressor p53 and estrogen receptor (ER) were originally characterized as nuclear transcription factors. In addition to their individual roles as regulators of various genes, these two proteins interact resulting in major cellular consequences. In addition to its nuclear role, p53 has been localized to the mitochondria where it executes various transcription-independent functions. Likewise, ERs are reported to be present in mitochondria; however their functional roles remain to be clearly defined. In this review, we provide an integrated view of the current knowledge of nuclear and mitochondrial p53 and ERs and how it relates to normal and pathological physiology.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026364PMC
http://dx.doi.org/10.1016/j.mito.2013.10.002DOI Listing

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