Ko

Lord et al., 2000; Nosaka etal., 1999; Hoover et al., 2001; Moon and Nelson, 2001; Moon et al., 2004a; Sugimoto et al., 2003 Fournier et al., 2005 Kobayashi et al., 2000 Tetsu etal., 1998; Guo et al., 2007

h aMethod (method used to demonstrate binding to the c-myc promoter): E = EMSA = electrophoretic mobility shift assay; D = DNAP = DNA precipitation assay; C = ChIP = chromatin immunoprecipitation assay; F = (DNAse I) footprinting analysis; M = methylation interference analysis; NMR = NMR (nuclear magnetic resonance) structure; MCA = missing contact analysis; FBA = filter binding assay; EPA = exonuclease protection assay; SW = Southwestern blot analysis; FRET = real-time FRET (fluorescence resonance energy transfer) assay; PP = potassium permanganate modification; OC = OP/Cu (orthophenanthroline/copper) footprinting; IB = immunoblotting of protein-DNA complexes; IP = immunoprecipitation of labeled oligonucleotides.

bComment: IV = in vitro = (partially) purified transcription factor; S = supershift experiments; C = competition experiments; P = binding site was point-mutated (or deleted). cExpression: T = transcript = mRNA = endogenous mRNA level affected; P = protein = endogenous protein level affected; RO = nuclear run-on or run-off transcription; CH = effect was detected in the presence of cycloheximide.

dManipulation of transcription factor: P = purified transcription factor; OE = overexpression of wild type; dn = dominant-negative form; ca = constitutively active form; del = analyzed with deletion (or/and point) mutants of the transcription factor; RNAi = RNA interference = knockdown (although mechanistically different siRNA, shRNA and antisense RNA approaches are listed as RNAi); tg = transgenic cells/mice; KO = knockout cells/mice (cancer cell lines deficient in transcription factor); A/R = activation/repression of the transcriptional activity of the transcription factor (see text for details).

eReporter contruct: T = transiently transfected; S = stably transfected; E = episomal vector; IV = in vitro transcription; M = microinjection into Xenopus laevis oocytes. fManipulation of binding site: wt = "wild type" c-myc promoter; del = analyzed with deletion mutants of c-myc promoter; P = binding site was point-mutated; H = binding site upstream (or downstream) of heterologous core promoter.

gME1a1/CT-l2, ME1a2, and the "E2F" binding site each represent overlapping binding sites for several transcription factors.

h^-Catenin, 7-catenin, and Notchl, which do not bind to DNA, serve as coactivators for their DNA-binding partner transcription factors TCF-4, LEF-1, or CSL, respectively, that act as repressors in the absence of their coactivators.

iIn addition to binding to their own genuine binding site, Smad1 and Smad3 were also found at a ^-catenin/TCF-4 binding site (TBE3 = TBE-A) while vice versa TCF-4 and ^-catenin were found at a Smad1 binding site (SBE-A), too. It is indicated in brackets, whether the data for Smad1, Smad3, TCF-4, and ^-catenin were obtained at their own genuine binding site or at the additional site, where Smads and ^-catenin/TCF-4/LEF-1 associate. Own genuine binding sites: SBE-A for Smad1; TIE for Smad3; TBE1, TBE2, TBE3 for TCF-4 and ^-catenin. Additional sites: TBE-A for Smad1; TBE3 for Smad3; SBE-A for TCF-4 and ^-catenin.

jAlbert etal. (2001) point-mutated the E2F binding site in the context of the wild-type c-myc promoter with an otherwise intact P2 promoter region. Krumm etal. (1995) deleted the E2F binding site in the context of a deletion mutant of the c-myc P2 promoter already lacking the P2 TATA-box and both Inr of the P2 promoter.

kSp3 slightly represses the human c-myc promoter in human HeLa cervix carcinoma cells, which contain endogenous Sp1 (Majello et al., 1995). Sp3 was reported to transactivate the human c-myc promoter in Sp1-deficient Drosophila Schneider SL2 cells (Majello et al., 1997), but coexpression of exogenous Sp1 restored the ability of Sp3 to repress the Sp1-mediated activity of the human c-myc promoter in these cells (Majello et al., 1995, 1997).

lMAZ binds to ME1a1/CT-I2, ME1a2, the CT-element (CT), and the c-myc attenuator (att) region within exon 1.

mMIBP1, RFX1, and HOXB4 bind to MIE1. In addition, MIBP1 and RFX1 bind also to 5'MIF, which is positioned 5' of the P1 transcription start site.

nIn addition to binding to the TIE, Smad4 binds also to a binding site adjacent to the TCF-4/LEF-1 binding site TBE1, where it associates with LEF-1. It is indicated in brackets whether the data for Smad4 were obtained at the TIE (TIE) or at this additonal Smad4 binding site adjacent to TBE1 (near TBE1).

transcriptional control (Marcu et al., 1992; Siebenlist et al., 1984). Well-characterized examples for deregulated c-myc transcription are Burkitt's lymphoma where a typical shift in promoter usage from P2 to P1 coincides with a loss of the block to transcriptional elongation (see Section IV.F).

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