Analysis of the DNA-binding activities of Myc/Max/Mad network complexes during induced differentiation of U-937 monoblasts and F9 teratocarcinoma cells

No abstract is available for this paper.

• Publication year

  1997

• Venue

  Oncogene

• Publication date

  1997-08-07

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/sj.onc.1201390PMID 9264414
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites.

  1997cited by this paper
• Rox, a novel bHLHZip protein expressed in quiescent cells that heterodimerizes with Max, binds a non‐canonical E box and acts as a transcriptional repressor

  1997cited by this paper
• Inhibition of cell proliferation by the Mad1 transcriptional repressor

  1996cited by this paper
• Proteins of the Myc network: essential regulators of cell growth and differentiation.

  1996cited by this paper
• Differential effects by Mad and Max on transformation by cellular and viral oncoproteins.

  1995cited by this paper
• Regulation of Myc and Mad during epidermal differentiation and HPV-associated tumorigenesis.

  1995cited by this paper
• Contrasting roles for Myc and Mad proteins in cellular growth and differentiation.

  1995cited by this paper
• Repression of Myc-Ras cotransformation by Mad is mediated by multiple protein-protein interactions.

  1995cited by this paper
• Mad3 and Mad4: novel Max‐interacting transcriptional repressors that suppress c‐myc dependent transformation and are expressed during neural and epidermal differentiation.

  1995cited by this paper
• Expression of the mad gene during cell differentiation in vivo and its inhibition of cell growth in vitro

  1995cited by this paper
• Transcriptional activation by Myc is under negative control by the transcription factor AP‐2.

  1995cited by this paper
• Differential regulation of Max and role of c-Myc during erythroid and myelomonocytic differentiation of K562 cells.

  1995cited by this paper
• Effects of the MYC oncogene antagonist, MAD, on proliferation, cell cycling and the malignant phenotype of human brain tumour cells

  1995cited by this paper
• Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3.

  1995cited by this paper
• Suppression of Myc, but not E1a, transformation activity by Max-associated proteins, Mad and Mxi1.

  1994cited by this paper
• Regulation of murine Max (Myn) parallels the regulation of c-Myc in differentiating murine erythroleukemia cells.

  1994cited by this paper
• Expression of mad, mxi1, max and c-myc during induced differentiation of hematopoietic cells: opposite regulation of mad and c-myc.

  1994cited by this paper
• Inhibition of transcriptional regulator Yin-Yang-1 by association with c-Myc.

  1993cited by this paper
• Direct role for Myc in transcription initiation mediated by interactions with TFII-I

  1993cited by this paper
• Mxi1, a protein that specifically interacts with Max to bind Myc-Max recognition sites.

  1993cited by this paper
• Mad: a heterodimeric partner for Max that antagonizes Myc transcriptional activity.

  1993cited by this paper
• Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.

  1993cited by this paper
• The c‐Myc protein induces cell cycle progression and apoptosis through dimerization with Max.

  1993cited by this paper
• Oncogenic activity of the c-Myc protein requires dimerization with Max.

  1993cited by this paper
• A switch from Myc:Max to Mad:Max heterocomplexes accompanies monocyte/macrophage differentiation.

  1993cited by this paper
• Identification of casein kinase II phosphorylation sites in Max: effects on DNA-binding kinetics of Max homo- and Myc/Max heterodimers.

  1993cited by this paper
• Sequence-specific transcriptional activation by Myc and repression by Max

  1993cited by this paper
• Max and c-Myc/Max DNA-binding activities in cell extracts.

  1992cited by this paper
• Myc and Max associate in vivo.

  1992cited by this paper
• Casein kinase II inhibits the DNA-binding activity of Max homodimers but not Myc/Max heterodimers.

  1992cited by this paper
• The regulation of transcription by phosphorylation.

  1992cited by this paper
• Biphasic effect of Max on Myc cotransformation activity and dependence on amino- and carboxy-terminal Max functions.

  1992cited by this paper
• myc function and regulation.

  1992cited by this paper
• Transcriptional activation by the human c-Myc oncoprotein in yeast requires interaction with Max

  1992cited by this paper
• Myc and Max proteins possess distinct transcriptional activities

  1992cited by this paper
• Interferon gamma abrogates the differentiation block in v-myc-expressing U-937 monoblasts.

  1991cited by this paper
• Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc.

  1991cited by this paper
• Methylation-sensitive sequence-specific DNA binding by the c-Myc basic region.

  1991cited by this paper
• Association of Myn, the murine homolog of max, with c-Myc stimulates methylation-sensitive DNA binding and ras cotransformation.

  1991cited by this paper
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  1990cited by this paper
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  1989cited by this paper
• Phorbol ester-induced terminal differentiation is inhibited in human U-937 monoblastic cells expressing a v-myc oncogene.

  1988cited by this paper
• c-myc and c-myb protein degradation: effect of metabolic inhibitors and heat shock

  1988cited by this paper
• Post-transcriptional control of myc and p53 expression during differentiation of the embryonal carcinoma cell line F9

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• Establishment of a near-tetraploid B-cell lymphoma line with duplication of the 8;14 translocation.

  1984cited by this paper
• Binding of a simian virus 40 T antigen-related protein to DNA.

  1981cited by this paper
• Expression of MLR-S in human myeloid, monocytic and erythroid cell differentiation.

  1980cited by this paper
• The induction of differentiation in teratocarcinoma stem cells by retinoic acid.

  1978cited by this paper
• Continuous growth and differentiation of human myeloid leukaemic cells in suspension culture

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• Establishment of tumor cell lines cultured from chickens with avian lymphoid leukosis.

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• Novel strategy to inhibit the oncogenic transcription factor c-Myc in triple-negative breast cancer

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• CXCL10 expression induced by Mxi1 inactivation induces mesangial cell apoptosis in mouse Habu nephritis.

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• Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.

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• Structural biology of transcriptional regulation in the c-Myc network

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• and decreased proteasome-mediated turnover c-Myc hot spot mutations in lymphomas result in inefficient ubiquitination

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• MAD1 and its life as a MYC antagonist: an update.

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• Protein Structure and Interaction in Health and Disease

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• TGF-beta enforces senescence in Myc-transformed hematopoietic tumor cells through induction of Mad1 and repression of Myc activity.

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• Regulation of the MAD1 promoter by G-CSF

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• The central domain of transcription factor FOXM1c directly interacts with itself in vivo and switches from an essential to an inhibitory domain depending on the FOXM1c binding site

  2007cites this paper
• Regulation of the potential tumorsuppressor gene mad1 by G-CSF

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• Structural aspects of interactions within the Myc/Max/Mad network.

  2006cites this paper
• FOXM1c is activated by cyclin E/Cdk2, cyclin A/Cdk2, and cyclin A/Cdk1, but repressed by GSK-3alpha.

  2006cites this paper
• The Mad side of the Max network: antagonizing the function of Myc and more.

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• Despite its strong transactivation domain, transcription factor FOXM1c is kept almost inactive by two different inhibitory domains

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• Regulation of RNA polymerase III transcription during differentiation.

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• Expression and DNA‐binding activity of MYCN/Max and Mnt/Max during induced differentiation of human neuroblastoma cells

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  2003cites this paper
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