ArticleMolecular and cellular biology1997
Function of the c-Myc antagonist Mad1 during a molecular switch from proliferation to differentiation.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 66 citations in OpenAlex.
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- TGFβ1 enhances MAD1 expression and stimulates promoter-bound Pol II phosphorylation: basic functions of C/EBP, SP and SMAD3 transcription factors.BMC molecular biology · 2011Article
- Myc inhibits p27-induced erythroid differentiation of leukemia cells by repressing erythroid master genes without reversing p27-mediated cell cycle arrest.Molecular and cellular biology · 2008Article
- Regulation of the MAD1 promoter by G-CSF.Nucleic acids research · 2008Article
- Mad4 is regulated by a transcriptional repressor complex that contains Miz-1 and c-Myc.The Biochemical journal · 2003Article
- Review
- MAD1 and p27(KIP1) cooperate to promote terminal differentiation of granulocytes and to inhibit Myc expression and cyclin E-CDK2 activity.Molecular and cellular biology · 2002Article
- A Myb dependent pathway maintains Friend murine erythroleukemia cells in an immature and proliferating state.Oncogene · 2002Article
- Article
- Function of RARalpha during the maturation of neutrophils.Oncogene · 2001Review
- S-phase-specific expression of the Mad3 gene in proliferating and differentiating cells.The Biochemical journal · 2001Article
- Targeted deletion of the S-phase-specific Myc antagonist Mad3 sensitizes neuronal and lymphoid cells to radiation-induced apoptosis.Molecular and cellular biology · 2001Article
- Article
- Mad1 function is regulated through elements within the carboxy terminus.Molecular and cellular biology · 2000Article
- Review
- Essential role for Max in early embryonic growth and development.Genes & development · 2000Article
- New Myc-interacting proteins: a second Myc network emerges.Oncogene · 1999Review
- Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation.The EMBO journal · 1998Article
- MXD1 is a Potential Prognostic Biomarker and Correlated With Specific Molecular Change and Tumor Microenvironment Feature in Esophageal Squamous Cell Carcinoma.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mad-Max heterodimers have been shown to antagonize Myc transforming activity by a mechanism requiring multiple protein-protein and protein-DNA interactions. However, the mechanism by which Mad functions in differentiation is unknown. Here, we present evidence that Mad functions by an active repression mechanism to antagonize the growth-promoting function(s) of Myc and bring about a transition from cellular proliferation to differentiation. We demonstrate that exogenously expressed c-Myc blocks inducer-mediated differentiation of murine erythroleukemia cells without disrupting the induction of endogenous Mad; rather, high levels of c-Myc prevent a heterocomplex switch from growth-promoting Myc-Max to growth-inhibitory Mad-Max. Cotransfection of a constitutive c-myc with a zinc-inducible mad1 results in clones expressing both genes, whereby a switch from proliferation to differentiation can be modulated. Whereas cells grown in N'N'-hexamethylene bisacetamide in the absence of zinc fail to differentiate, addition of zinc up-regulates Mad expression by severalfold and differentiation proceeds normally. Coimmunoprecipitation analysis reveals that Mad-Max complexes are in excess of Myc-Max in these cotransfectants. Moreover, we show that the Sin-binding, basic region, and leucine zipper motifs are required for Mad to function during a molecular switch from proliferation to differentiation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.