The role of c-myc in cell growth
References and recommended reading (68)
- et al.
Control of c-myc Regulation in Normal and Neoplastic Cells
Adv Cancer Res
(1991) - et al.
Myc and Max: a Putative Transcriptional Complex in Search of a Cellular Target
Curr Opin Cell Biol
(1992) - et al.
Max and c-Myc/Max DNA Binding Activities in Cell Extracts
Oncogene
(1992) - et al.
IL-2 and EGF Receptor Stimulate the Hematopoietic Cell Cycle via Different Signalling Pathways: Demonstration of a Novel Role for c-myc
Cell
(1992) - et al.
Cascade Induction of c-fos, c-myc, and Heat Shock 70K Transcripts during Regression of the Rat Ventral Prostate Gland
Mol Endocrinol
(1988) - et al.
Nuclear Events after Activation of CD4+8+ Thymocytes
J Immunol
(1990) - et al.
Cooperative Interaction Between c-myc and bcl-2 Proto-oncogenes
Nature
(1992) - et al.
Domains of Human c-myc Protein Required for Autosuppression and Cooperation with ras Oncogenes are Overlapping
Mol Cell Biol
(1990) - et al.
Induction of Apoptosis in Fibroblasts by c-myc Protein
Cell
(1992) - et al.
Definition of Regions in Human c-myc that are Involved in Transformation and Nuclear Localization
Mol Cell Biol
(1987)
Sequence-specific DNA Binding by the c-Myc Protein
Science
Methylation-sensitive Sequence-specific DNA Binding by the c-Myc Basic Region
Science
Max: a Helix-loop-helix Zipper Protein that Forms a Sequence-specific DNA-binding Complex with Myc
Science
Association of Myn, the Murine Homolog of Max, with c-Myc Stimulates Methylation-sensitive DNA Binding and ras Cotransformation
Cell
Intracellular Leucine Zipper Interactions Suggest c-Myc Hetero-oligomerization
Mol Cell Biol
Determination of the c-Myc DNA-binding Site
max Encodes a Sequence-specific DNA-binding Protein and is not Regulated by Serum Growth Factors
Oncogene
Expression, Regulation and Chromosomal Localization of the Max Gene
Myc and Max Associate in vivo
Genes Dev
Transcriptional Activation by c-Myc Oncoprotein in Yeast Requires Interaction with Max
Nature
Mutational Analysis of Max: Role of Basic, Helix-loop-helix/Leucine Zipper Domains in DNA Binding, Dimerization and Regulation of Myc-mediated Transcriptional Activation
Oncogene
Max: Functional Domains and Interaction with c-Myc
Genes Dev
The N-Myc Oncoprotein is Associated in Vivo with the Phosphoprotein Max (p20/p22) in Human Neuroblastoma Cells
EMBO J
Myc and Max Possess Distinct Transcriptional Activities
Nature
Myc Family Oncoproteins Function through a Common Pathway to Transform Normal Cells in Culture: Cross-interference by Max and Trans-activating Dominant Mutants
Genes Dev
Alternative Forms of Max as Enhancers or Suppressors of Myc-Ras Cotransformation
Science
c-myc Protein Expression in Untransformed Fibroblasts
Oncogene
Casein Kinase II Inhibits the DNA-binding Activity of Max Homodimers but not Myc/Max Heterodimers
Genes Dev
Cell Specific Regulation of the c-myc Gene by Lymphocyte Mitogens and Platelet-derived Growth Factor
Cell
Growth Factor-responsive Genes in Fibroblasts
Cell Growth Differentiation
C-myc Oncogene Protein Synthesis is Independent of the Cell Cycle in Human and Avian Cells
Nature
Metabolism of c-myc Gene Products: c-myc mRNA and Protein Expression in the Cell Cycle
EMBO J
Levels of c-myc Oncogene mRNA are Invariant Throughout the Cell Cycle
Nature
The Myc Protein Activates Transcription of the Alpha-prothymosin Gene
EMBO J
Cited by (383)
SOX2 and squamous cancers
2020, Seminars in Cancer BiologyCitation Excerpt :This should not be surprising. Over 25 years ago it was demonstrated that deregulation of the proto-oncogene (and Yamanaka factor) c-MYC has very different phenotypic impacts on the same cells (apoptosis or proliferation) depending on the culture conditions [74]. Further work in the mouse showed that c-Myc can induce apoptosis via upregulation of the p19Arf tumour suppressor gene which triggers p53 [90]; and that the level of expression of Myc in vivo governs the phenotypic impact, so that overexpression triggers the Arf-p53 axis while physiological levels of Myc, when persistent can drive oncogenesis without engaging Arf-p53 [91].
XPO1 is a critical player for bortezomib resistance in multiple myeloma: A quantitative proteomic approach
2019, Journal of ProteomicsNano-Assembly of Pamitoyl-Bioconjugated Coenzyme-A for Combinatorial Chemo-Biologics in Transcriptional Therapy
2018, Bioconjugate ChemistryIs Myc an Important Biomarker? Myc Expression in Immune Disorders and Cancer
2018, American Journal of the Medical SciencesMxi1 and Mxi1-0 antagonize N-Myc function and independently mediate apoptosis in neuroblastoma
2015, Translational OncologyCitation Excerpt :Although MYCN clearly serves as a marker for advanced NB [6], the precise mechanisms by which MYCN and deregulated N-Myc protein contribute to the pathogenesis of NB remain poorly understood. N-Myc belongs to the basic helix-loop-helix leucine zipper (b-HLH-LZ) superfamily and to the MYC family of proto-oncogenes that act as transcriptional activators of growth-related target genes [7,8]. Myc proteins dimerize with the ubiquitously expressed Max protein, bind to CACGTG (E-box) sequences [9–11], and regulate cell proliferation and differentiation [7,12–17], cell cycle control [18–20], and apoptosis [21–24].