Myc-Max-Mad: a transcription factor network controlling cell cycle progression, differentiation and death.
暂无分享,去创建一个
B. Amati | H. Land | H Land | B Amati | Bruno Amati | Hartmut Land
[1] C. Dang,et al. Max: functional domains and interaction with c-Myc. , 1992, Genes & development.
[2] G. Prendergast,et al. A new bind for Myc. , 1992, Trends in genetics : TIG.
[3] P. Leder,et al. An embryonically expressed gene is a target for c-Myc regulation via the c-Myc-binding sequence. , 1992, Genes & development.
[4] M. Cole,et al. Casein kinase II inhibits the DNA-binding activity of Max homodimers but not Myc/Max heterodimers. , 1992, Genes & development.
[5] M. Birrer,et al. Regions within the c-Myc protein that are necessary for transformation are also required for inhibition of differentiation of murine erythroleukemia cells. , 1992, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[6] G. Evan,et al. Transcriptional activation by the human c-Myc oncoprotein in yeast requires interaction with Max , 1992, Nature.
[7] V. Rotter,et al. c-Myc trans-activates the p53 promoter through a required downstream CACGTG motif. , 1993, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[8] R. DePinho,et al. Myc family oncoproteins function through a common pathway to transform normal cells in culture: cross-interference by Max and trans-acting dominant mutants. , 1992, Genes & development.
[9] Bruno Amati,et al. Oncogenic activity of the c-Myc protein requires dimerization with Max , 1993, Cell.
[10] M. Pagano,et al. Differential modulation of cyclin gene expression by MYC. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[11] N. Hay,et al. c-Myc induces the expression and activity of ornithine decarboxylase. , 1993, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[12] M. Raffeld,et al. Clustered mutations in the second exon of the MYC gene in sporadic Burkitt's lymphoma. , 1993, Oncogene.
[13] G. Klein,et al. Phosphorylation sites mapping in the N-terminal domain of c-myc modulate its transforming potential. , 1993, Oncogene.
[14] G. Evan,et al. Domains of human c-myc protein required for autosuppression and cooperation with ras oncogenes are overlapping , 1990, Molecular and cellular biology.
[15] A. Rustgi,et al. Amino-terminal domains of c-myc and N-myc proteins mediate binding to the retinoblastoma gene product , 1991, Nature.
[16] A. Patel,et al. myc function and regulation. , 1992, Annual review of biochemistry.
[17] E. Reddy,et al. Mutational analysis of Max: role of basic, helix-loop-helix/leucine zipper domains in DNA binding, dimerization and regulation of Myc-mediated transcriptional activation. , 1992, Oncogene.
[18] Gerard I. Evan,et al. Induction of apoptosis in fibroblasts by c-myc protein , 1992, Cell.
[19] Stephen K. Burley,et al. Recognition by Max of its cognate DNA through a dimeric b/HLH/Z domain , 1993, Nature.
[20] V. Pirrotta,et al. Multimerization of the Drosophila zeste protein is required for efficient DNA binding. , 1993, The EMBO journal.
[21] M. Cole,et al. max encodes a sequence-specific DNA-binding protein and is not regulated by serum growth factors. , 1992, Oncogene.
[22] J A Moshier,et al. Transformation of NIH/3T3 cells by ornithine decarboxylase overexpression. , 1993, Cancer research.
[23] W. Gu,et al. Opposite regulation of gene transcription and cell proliferation by c-Myc and Max. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[24] L. Andersson,et al. Ornithine decarboxylase activity is critical for cell transformation , 1992, Nature.
[25] M. Henriksson,et al. Identification of casein kinase II phosphorylation sites in Max: effects on DNA-binding kinetics of Max homo- and Myc/Max heterodimers. , 1993, Oncogene.
[26] D. Gillespie,et al. Transcription activation by Myc and Max: flanking sequences target activation to a subset of CACGTG motifs in vivo. , 1993, The EMBO journal.
[27] B. Amati,et al. Distinct DNA binding preferences for the c-Myc/Max and Max/Max dimers. , 1993, Nucleic acids research.
[28] G. Evan,et al. Max and c-Myc/Max DNA-binding activities in cell extracts. , 1992, Oncogene.
[29] J. Woodgett,et al. Site-specific modulation of c-Myc cotransformation by residues phosphorylated in vivo. , 1994, Oncogene.
[30] K. Alitalo,et al. Alternative Forms of Max as Enhancers or Suppressors of Myc-Ras Cotransformation , 1992, Science.
[31] K. Klempnauer,et al. Sequence-specific DNA binding by Myc proteins. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[32] R. DePinho,et al. Myc and Max: a putative transcriptional complex in search of a cellular target. , 1992, Current opinion in cell biology.
[33] R. Eisenman,et al. Myc and Max proteins possess distinct transcriptional activities , 1992, Nature.
[34] R. Davis,et al. Cell cycle regulation of the c-Myc transcriptional activation domain , 1993, Molecular and cellular biology.
[35] R. Brent,et al. Mxi1, a protein that specifically interacts with Max to bind Myc-Max recognition sites , 1993, Cell.
[36] H. Varmus,et al. Definition of regions in human c-myc that are involved in transformation and nuclear localization , 1987, Molecular and cellular biology.
[37] C. Goding,et al. C-myc and the yeast transcription factor PHO4 share a common CACGTG-binding motif. , 1991, Oncogene.
[38] M. Obinata,et al. Functional domains of c-Myc involved in the commitment and differentiation of murine erythroleukemia cells. , 1993, Oncogene.
[39] D. Gillespie,et al. Gene-regulatory properties of Myc helix-loop-helix/leucine zipper mutants: Max-dependent DNA binding and transcriptional activation in yeast correlates with transforming capacity. , 1993, Oncogene.
[40] R. Eisenman,et al. Mad: A heterodimeric partner for Max that antagonizes Myc transcriptional activity , 1993, Cell.
[41] R. Eisenman,et al. Myc and Max associate in vivo. , 1992, Genes & development.
[42] H. Weintraub,et al. Sequence-specific DNA binding by the c-Myc protein. , 1990, Science.
[43] G. Prendergast,et al. Association of Myn, the murine homolog of Max, with c-Myc stimulates methylation-sensitive DNA binding and ras cotransformation , 1991, Cell.
[44] S. Goff,et al. Inhibition of transcriptional regulator Yin-Yang-1 by association with c-Myc. , 1993, Science.
[45] G. Evan,et al. The c‐Myc protein induces cell cycle progression and apoptosis through dimerization with Max. , 1993, The EMBO journal.
[46] H. Hibshoosh,et al. Effects of overexpression of ornithine decarboxylase (ODC) on growth control and oncogene-induced cell transformation. , 1991, Oncogene.
[47] R. Eisenman,et al. A switch from Myc:Max to Mad:Max heterocomplexes accompanies monocyte/macrophage differentiation. , 1993, Genes & development.
[48] C. Dang,et al. Activation domains of L-Myc and c-Myc determine their transforming potencies in rat embryo cells , 1992, Molecular and cellular biology.
[49] R. Roeder,et al. Direct role for Myc in transcription initiation mediated by interactions with TFII-I , 1993, Nature.
[50] I. Magrath,et al. Point mutations in the c–Myc transactivation domain are common in Burkitt's lymphoma and mouse plasmacytomas , 1993, Nature Genetics.
[51] G. Prendergast,et al. Methylation-sensitive sequence-specific DNA binding by the c-Myc basic region. , 1991, Science.
[52] J L Cleveland,et al. The ornithine decarboxylase gene is a transcriptional target of c-Myc. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[53] M. Mori,et al. Prothymosin-α mRNA expression correlates with that of c-myc in human colon cancer , 1993 .
[54] D. Gillespie,et al. The leucine zipper domain of avian cMyc is required for transformation and autoregulation. , 1990, Oncogene.
[55] C. Dang,et al. B-myc inhibits neoplastic transformation and transcriptional activation by c-myc , 1993, Molecular and cellular biology.
[56] J. Lautenberger,et al. Sequence curiosity in v-myc oncogene , 1985, Nature.
[57] L. J. Veer,et al. TATA-binding protein and the retinoblastoma gene product bind to overlapping epitopes on c-Myc and adenovirus E1A protein. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[58] L. Larsson,et al. Expression of mad, mxi1, max and c-myc during induced differentiation of hematopoietic cells: opposite regulation of mad and c-myc. , 1994, Oncogene.
[59] N. Hay,et al. Sequence-specific transcriptional activation by Myc and repression by Max , 1993, Molecular and cellular biology.
[60] T. Graf,et al. The transforming activity of the chicken c-myc gene can be potentiated by mutations. , 1987, Oncogene.
[61] G. Prendergast,et al. Biphasic effect of Max on Myc cotransformation activity and dependence on amino- and carboxy-terminal Max functions. , 1992, Genes & development.
[62] M. Schwab,et al. The N‐Myc oncoprotein is associated in vivo with the phosphoprotein Max(p20/22) in human neuroblastoma cells. , 1991, The EMBO journal.
[63] A. Baxevanis,et al. Interactions of coiled coils in transcription factors: where is the specificity? , 1993, Current opinion in genetics & development.
[64] J. Bishop,et al. The MYC protein activates transcription of the alpha‐prothymosin gene. , 1991, The EMBO journal.
[65] J. Barrett,et al. An amino-terminal c-myc domain required for neoplastic transformation activates transcription , 1990, Molecular and cellular biology.
[66] G. Evan,et al. The role of c-myc in cell growth. , 1993, Current opinion in genetics & development.