Myc's broad reach.

By M. Eilers, R. Eisenman. Genes & Development, 2008

958 citations recorded by the source corpus.

The role of the myc gene family in the biology of normal and cancer cells has been intensively studied since the early 1980s. myc genes, responding to diverse external and internal signals, express transcription factors (c-, N-, and L-Myc) that heterodimerize with Max, bind DNA, and modulate expression of a specific set of target genes. Over the last few years, expression profiling, genomic binding studies, and genetic analyses in mammals and Drosophila have led to an expanded view of Myc function. This review is focused on two major aspects of Myc: the nature of the genes and pathways that are targeted by Myc, and the role of Myc in stem cell and cancer biology.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/87eee7bb598b5d067eb24e693df08002119cd2de

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Citations in the corpus

MYC as a regulator of ribosome biogenesis and protein synthesis (2010, background): “The selective poly(ADP-ribose) polymerase-1(2) inhibitor, CEP-8983, increases the”
Glutamine Addiction: A New Therapeutic Target in Cancer (2010, background): “Myc is a basic helix–loop–helix zipper (bHLHZ) protein that heterodimerizes with the small bHLHZ protein MAX and exerts both activating and repressing transcriptional effects [36].”
The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation (2011, background): “Consistent with a direct role ofMyc in regulating cell proliferation (Dang et al., 2006; Eilers and Eisenman, 2008), addition of a-KG with HT and PAs failed to promote cell proliferation in Myc-deficient T cells (Figure S7C).”
Transcriptional Amplification in Tumor Cells with Elevated c-Myc (2012, positive): “…angiogenesis, among others (Amati et al., 1998; Amati et al., 2001; Cole and Cowling, 2008; Cowling and Cole, 2010; Dai and Lu, 2008; Dang, 2010; Eilers and Eisenman, 2008; Facchini and Penn, 1998; Gallant, 2005; Hanahan and Weinberg, 2011; Herold et al., 2009; Hoffman and Liebermann, 2008;…”
Myc and cell cycle control. (2015, background): “However Myc has also the ability to repress genes although the mechanisms are less well known (for recent reviews see [31–34]).”
c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells (2012, neutral): “These complex patterns of binding, expression, and function, typical for studies of this oncogene (Chen et al., 2008; Dang, 2010; Eilers and Eisenman, 2008; Ji et al., 2011), failed to illuminate a principle for Myc action.”
Quantitative interaction proteomics and genome-wide profiling of epigenetic histone marks and their readers. (2010, background): “Since c-Myc is expressed in a broad spectrum of proliferating cell types (Eilers and Eisenman, 2008; Meyer and Penn, 2008), and has been shown to bind P-TEFb and stimulate elongation at a set of genes in tumor cells (Eberhardy and Farnham, 2001, 2002; Gargano et al.”
MYC-induced Cancer Cell Energy Metabolism and Therapeutic Opportunities (2009, background): “The finding that Myc could regulate transcription mediated by RNA polymerases I (for rRNA transcription) and III (for tRNA and small RNA transcription), in addition to RNA Pol II, further shows its role in biogenesis of ribosomes (4, 5, 21).”
Targeting MYC dependence in cancer by inhibiting BET bromodomains (2011, background): “MYC is a member of a related family of transcription factors that also includes MYCN and MYCL (22, 23).”
c-Myc regulates transcriptional pause release (2010, background): “Inhibition of c-Myc/Max function leads to a substantial reduction in the levels of Ser2-phosphorylated Pol II in cells, which is the form associated with elongation, but does not affect the levels of Ser5-phos-phorylated Pol II, which is the form associated with initiation. c-Myc binds P-TEFb, which”
c-Myc and Cancer Metabolism (2012, positive): “The c-Myc heterodimer can also repress gene expression via binding to the transcription factor Miz1 (38, 39).”