c-MYC apoptotic function is mediated by NRF-1 target genes

Morrish, Fionnuala; Giedt, Christopher D.; Hockenbery, David M.

doi:10.1101/gad.1032503

Cited by 112 publications

(116 citation statements)

References 63 publications

Supporting

Mentioning

109

Contrasting

Unclassified

Order By: Relevance

“…Indeed, one pathway through which p53 can directly regulate mitochondrial oxygen consumption is by transactivation of SCO2, an assembly factor for cytochrome c oxidase (9). Similarly, other tumor suppressors and oncogenes such as c-myc can also regulate key components of mitochondrial function such as cytochrome c (10). Such regulation may suggest that the handful of genes commonly altered or deleted in human tumors might ultimately provide the genetic link between mitochondria function and cell-cycle checkpoints.…”

Section: Figmentioning

confidence: 99%

The Krebs cycle meets the cell cycle: Mitochondria and the G ₁ –S transition

Finkel

Hwang

2009

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Section: Figmentioning

confidence: 99%

The Krebs cycle meets the cell cycle: Mitochondria and the G ₁ –S transition

Finkel

Hwang

2009

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

“…NRF-1 regulates MEF2A in muscle possibly accounting for indirect NRF-1 control over the expression of musclespecific MEF2 target genes [33]. Finally, c-myc acts on the expression of certain NRF-1 target genes through a canonical NRF-1 binding site resulting in the sensitization of cells to apoptosis [34]. Expression of a dominant-negative allele of NRF-1 blocked the induction of apoptosis by c-myc.…”

Section: Transcription Factors Acting Upon the Nuclear Genomementioning

confidence: 99%

“…. Finally, c-myc acts on the expression of certain NRF-1 target genes through a canonical NRF-1 binding site resulting in the sensitization of cells to apoptosis [34]. Expression of a dominant-negative allele of NRF-1 blocked the induction of apoptosis by c-myc.…”

Section: Transcription Factors Acting Upon the Nuclear Genomementioning

confidence: 99%

7.3 Transcriptional Integration of Mitochondrial Biogenesis

Scarpulla¹

2007

Handbook of Neurochemistry and Molecular Neurobiology

View full text Add to dashboard Cite

Gene regulatory factors encoded by the nuclear genome are essential for mitochondrial biogenesis and function. Some of these factors act exclusively within the mitochondria to regulate the control of mitochondrial transcription, translation and other functions. Others govern the expression of nuclear genes required for mitochondrial metabolism and organelle biogenesis. The peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family of transcriptional coactivators plays a major role in transducing and integrating physiological signals governing metabolism, differentiation and cell growth to the transcriptional machinery controlling mitochondrial functional capacity. Thus, the PGC-1 coactivators serve as a central component of the transcriptional regulatory circuitry that coordinately controls the energy-generating functions of mitochondria in accordance with the metabolic demands imposed by changing physiological conditions, senescence, and disease. KeywordsMitochondria; Peroxisome proliferator-activated receptor gamma coactivator 1 (PGC-1); Peroxisome proliferator-activated receptor (PPAR); transcription; gene regulation; metabolism Regulation of mitochondrial biogenesisA set of nuclear-encoded factors coordinately regulate mitochondrial mass and function in response to a host of energy and growth demands, including cellular metabolic stress, such as the constant production of reactive oxygen species (ROS). Dysregulation of mitochondrial function has broad implications for human disease including diabetes, heart failure and neurodegeneration. Thus, there is a high level of interest in developing therapeutic strategies aimed at modulating the regulatory pathways that control mitochondrial function and biogenesis. The nuclear-encoded transcription factors and coactivators that govern mitochondrial function serve as one major focus. Here we review recent advances in our understanding of this regulatory circuitry and its potential role in integrating mitochondrial biogenesis with cellular stress responses. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The transcription and translation of the mitochondrial genome is dependent upon a host of nuclear-encoded gene products (Figure 1; Box 1). Mitochondrial DNA (mtDNA) transcription requires a single RNA polymerase (POLRMT, see glossary) that shares sequence similarity with yeast mitochondrial and T3/T7 bacteriophage polymerases, two stimulatory transcription factors (Tfam, TFB2M) and a termination factor (MTERF1) [1,2]. Transcription occurs bi-directionally from divergent promoters termed LSP and HSP wi...

show abstract

“…Given the important role of NO as a second messenger, this mechanism thus may connect cytoplasmic signaling with the regulation of mitochondrial processes. Most recently, it has been shown that NRF-1 regulated genes are also functional targets of the oncogene class transcription factor c-Myc [42]. c-Myc expression is rapidly induced by mitogenic signaling [43], and it is possible that this physiological response may establish a link between mitogen signaling and mitochondrial biogenesis.…”

Section: Long-term Adjustmentsmentioning

confidence: 99%

Regulating cell survival by controlling cellular energy production: novel functions for ancient signaling pathways?

et al. 2004

View full text Add to dashboard Cite

Cell survival is maintained by growth factors and critically depends on sufficient energy supply. New evidence suggests that a rise in cellular energy production is not merely a homeostatic response to increased demand but subject to regulation by extrinsic factors. The mechanisms operating in this control are largely enigmatic. Work on transformed cells identified direct targeting of glycolytic enzymes by signaling proteins as one possibility. But mitochondrial oxidative phosphorylation and biogenesis may also be subject to regulation by growth and survival factors. Both, positive and negative regulators of cell survival impinge on the processes of cellular energy production to regulate growth and survival versus death.

show abstract

c-MYC apoptotic function is mediated by NRF-1 target genes

Cited by 112 publications

References 63 publications

The Krebs cycle meets the cell cycle: Mitochondria and the G ₁ –S transition

The Krebs cycle meets the cell cycle: Mitochondria and the G ₁ –S transition

7.3 Transcriptional Integration of Mitochondrial Biogenesis

Regulating cell survival by controlling cellular energy production: novel functions for ancient signaling pathways?

Contact Info

Product

Resources

About

c-MYC apoptotic function is mediated by NRF-1 target genes

Cited by 112 publications

References 63 publications

The Krebs cycle meets the cell cycle: Mitochondria and the G 1 –S transition

The Krebs cycle meets the cell cycle: Mitochondria and the G 1 –S transition

7.3 Transcriptional Integration of Mitochondrial Biogenesis

Regulating cell survival by controlling cellular energy production: novel functions for ancient signaling pathways?

Contact Info

Product

Resources

About

The Krebs cycle meets the cell cycle: Mitochondria and the G ₁ –S transition

The Krebs cycle meets the cell cycle: Mitochondria and the G ₁ –S transition