Transcriptional regulation and transformation by Myc proteins

By Sovana Adhikary, M. Eilers. Nature reviews. Molecular cell biology, 2005

1,221 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/5e48006e7c54c41bc4fd6d42c4530f78c2f11bd1

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Citations in the corpus

Transcriptional paradigms in mammalian mitochondrial biogenesis and function. (2008, background): “Thus it is thought that only a minority of genes bound by Myc/MAX are actually regulated by c-Myc (1).”
HIF-2alpha promotes hypoxic cell proliferation by enhancing c-myc transcriptional activity. (2007, background): “c-Myc is a basic-helix-loop-helix/leucine zipper (bHLH/ LZ) transcription factor that controls the G1-S cell-cycle transition and is overexpressed in many human tumors (Adhikary and Eilers, 2005; Nilsson and Cleveland, 2003).”
Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. (2006, background): “The c-Myc protein has many downstream targets that enhance proliferation and transformation (Adhikary and Eilers, 2005), many of which may have roles in the generation of iPS cells.”
MYC as a regulator of ribosome biogenesis and protein synthesis (2010, background): “All three Myc genes encode nuclear phosphoproteins that function as sequence-specific transcription factors that target a large number of genes, including many involved in the control of proliferation, growth, apoptosis, metabolism, adhesion, angiogenesis, DNA repair and protein synthesis (reviewed ”
Myc's broad reach. (2008, background): “E-box binding by Myc-Max has been predominantly associated with gene activation—a finding consistent with Myc’s ability to recruit multiple coactivator complexes (for reviews, see Grandori et al. 2000; Adhikary and Eilers 2005; Cole and Nikiforov 2006).”
The ERK1/2 mitogen-activated protein kinase pathway as a master regulator of the G1- to S-phase transition (2007, background): “In addition, c-Myc also impacts profoundly on cell growth by activating genes Oncogene encoding ribosomal proteins and translation factors (Adhikary and Eilers, 2005), and by stimulating transcription of ribosomal RNA genes by Pol I (Arabi et al., 2005; Grandori et al., 2005).”
p53 represses c-Myc through induction of the tumor suppressor miR-145 (2009, background): “In particular, c-Myc is a well known oncogene that plays an important role in neoplastic transformation and apoptosis (20) and can be negatively regulated by p53 (1).”
Hypoxia-Inducible Factor 1 and Dysregulated c-Myc Cooperatively Induce Vascular Endothelial Growth Factor and Metabolic Switches Hexokinase 2 and Pyruvate Dehydrogenase Kinase 1 (2007, background): “The transcriptional network of c-Myc, a basic helix-loop-helix transcription factor that heterodimerizes with Max, has been linked to many biological processes including development, cellular proliferation and growth, cell cycle, apoptosis, and energy metabolism (1, 8, 12, 27, 58).”
Strategies and new developments in the generation of patient-specific pluripotent stem cells. (2007, background): “The N terminus of Myc binds to several proteins, including TRRAP, which are components of the TIP60 and GCN5 histone acetyltransferase complexes, and TIP48 and TIP49, which contain ATPase domains (Adhikary and Eilers, 2005).”
HIF and c-Myc: sibling rivals for control of cancer cell metabolism and proliferation. (2007, background): “While c-Myc genomic amplification and translocation gives rise to extremely high protein levels, its upregulation more typically results from altered signal transduction and is therefore more modest (Nilsson and Cleveland, 2003). c-Myc acts as both a transcriptional activator and repressor, promotin”
Targeting oncogenic Myc as a strategy for cancer treatment (2018, background): “TARGETING THE MYC–MAX COMPLEX The Myc–Max complex is required for the binding of Myc to DNA and its subsequent activation of target gene transcription.(1) The Myc–Max dimer interface is a parallel, left-handed, four-helix bundle, with each monomer comprising two R-helices separated by a loop.”
Direct observation of individual endogenous protein complexes in situ by proximity ligation (2006, background): “The induction of transcription of Myc-regulated genes depends on chromatin remodeling at the promoters by the c-Myc complex, while RNA polymerase II may be recruited through the Akt pathwa”
The interplay between MYC and HIF in cancer (2008, background): “A significant amount of work on MYC has focused on cell-autonomous oncogenic alterations without adequate attention being paid to the hypoxic tumour microenvironmen”