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MYC oncogenes and human neoplastic disease
TLDR
Data is indicated that these oncoproteins actually serve quite different roles in vivo, indicating that the deregulated expression of each MYC gene is reproducibly associated with only certain naturally occurring malignancies in humans and that these genes are not interchangeable with respect to their aberrant functional consequences.
Myc-Induced T Cell Leukemia in Transgenic Zebrafish
TLDR
Visualization of leukemic cells expressing a chimeric transgene encoding Myc fused to green fluorescent protein (GFP) revealed that leukemias arose in the thymus, spread locally into gill arches and retro-orbital soft tissue, and then disseminated into skeletal muscle and abdominal organs.
Low molecular weight inhibitors of Myc–Max interaction and function
TLDR
The results show that the yeast two-hybrid screen is useful for identifying compounds that can be exploited in mammalian cells and provides a means by which structural analogs, based upon these first-generation Myc–Max inhibitors, can be developed to enhance antitumor efficacy.
Differential Interactions of Id Proteins with Basic-Helix-Loop-Helix Transcription Factors*
TLDR
The Id proteins display a signature range of interactions with all of their potential dimerization partners and may play a role in myogenesis which is distinct from that in hematopoiesis, as well as disrupting the ability of E protein-MyoD complexes to transactivate from a muscle creatine kinase reporter construct in vivo.
Multiple independent binding sites for small-molecule inhibitors on the oncoprotein c-Myc.
TLDR
All seven of the originally identified Myc inhibitors are shown to bind to one of these three discrete sites within the 85-residue bHLHZip domain of c-Myc, suggesting the widespread existence of peptide regions prone to small-molecule binding within ID domains.
Constitutive expression of a c-myb cDNA blocks Friend murine erythroleukemia cell differentiation.
TLDR
The results indicate that constitutive expression of a nontruncated human c-myb cDNA can exert profound effects on erythroid differentiation and argue for a causal role of c- myb in the F-MEL differentiation process.
C-MYC overexpression is required for continuous suppression of oncogene-induced senescence in melanoma cells
TLDR
One of the major functions of C-MYC overexpression in melanoma progression is to continuous suppress BRAFV600E- or NRASQ61R-dependent senescence programs, which agrees with the generally higher rates of activating mutations in BRAF than NRAS gene in human cutaneous melanomas.
Regulation of reactive oxygen species, DNA damage, and c-Myc function by peroxiredoxin 1
TLDR
It is suggested that increased DNA damage and tumor susceptibility in prdx1−/− animals results from this shift in intracellular ROS, which should be useful in studying the role of oxidative DNA damage in the causation of cancer and its prevention by antioxidants.
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