Regulated expression and function of the c-Myc antagonist, Mad1, during a molecular switch from proliferation to differentiation.
Cultraro
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CM
NCI-Navy Medical Oncology Branch, National Cancer Institute, NIH, Bethesds, MD, USA.
Bino
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T
Segal
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D000818:Animals; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D002454:Cell Differentiation / Q000235:genetics / Q000502:physiology; D002455:Cell Division / Q000235:genetics / Q000502:physiology; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000502:physiology*; D015972:Gene Expression Regulation, Neoplastic; D016259:Genes, myc; D004915:Leukemia, Erythroblastic, Acute / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D051379:Mice; D012097:Repressor Proteins; D014162:Transfection; D014407:Tumor Cells, Cultured
D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D004268:DNA-Binding Proteins; C079439:MXD1 protein, human; C499479:Mad protein, mouse; D012097:Repressor Proteins