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Myc-Induced T Cell Leukemia in Transgenic Zebrafish
The zebrafish is an attractive model organism for studying cancer development because of its genetic accessibility. Here we describe the induction of clonally derived T cell acute lymphoblasticExpand
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MYC oncogenes and human neoplastic disease
c-myc, N-myc and L-myc are the three members of the myc oncoprotein family whose role in the pathogenesis of many human neoplastic diseases has received wide empirical support. In this review, weExpand
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Low molecular weight inhibitors of Myc–Max interaction and function
c-Myc is helix–loop–helix–leucine zipper (HLH–ZIP) oncoprotein that is frequently deregulated in human cancers. In order to bind DNA, regulate target gene expression, and function in a biologicalExpand
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Tumor necrosis factor-alpha induction of novel gene products in human endothelial cells including a macrophage-specific chemotaxin.
Cytokines such as tumor necrosis factor alpha (TNF) profoundly affect endothelial cell function, promoting for example interaction with leukocytes and inducing a procoagulant phenotype. Changes ofExpand
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Structural rationale for the coupled binding and unfolding of the c-Myc oncoprotein by small molecules.
The basic-helix-loop-helix-leucine-zipper domains of the c-Myc oncoprotein and its obligate partner Max are intrinsically disordered (ID) monomers that undergo coupled folding and binding uponExpand
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Differential Interactions of Id Proteins with Basic-Helix-Loop-Helix Transcription Factors*
Dimerization of three Id proteins (Id1, Id2, and Id3) with the four class A E proteins (E12, E47, E2-2, and HEB) and two groups of class B proteins, the myogenic regulatory factors (MRFs: MyoD,Expand
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Multiple independent binding sites for small-molecule inhibitors on the oncoprotein c-Myc.
Deregulation of the c-Myc transcription factor is involved in many types of cancer, making this oncoprotein an attractive target for drug discovery. One approach to its inhibition has been to disruptExpand
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Pten mediates Myc oncogene dependence in a conditional zebrafish model of T cell acute lymphoblastic leukemia
Loss-of-function mutations in pten genes, or expression of a constitutively active version of Akt2, render T-ALL cell survival and disease progression independent of Myc.
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Constitutive expression of a c-myb cDNA blocks Friend murine erythroleukemia cell differentiation.
A full-length human c-myb cDNA clone has been isolated from a CCRF-CEM leukemia cell cDNA library. The plasmid vector contains simian virus 40-derived promotor, splice, and polyadenylation sequencesExpand
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Regulation of reactive oxygen species, DNA damage, and c-Myc function by peroxiredoxin 1
Overexpression of c-Myc results in transformation and multiple other phenotypes, and is accompanied by the deregulation of a large number of target genes. We previously demonstrated thatExpand
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