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Recognition of Local DNA Structures by p53 Protein
Abstract
p53 plays critical roles in regulating cell cycle, apoptosis, senescence and metabolism and is commonly mutated in human cancer. These roles are achieved by interaction with other proteins, but particularly by interaction with DNA. As a transcription factor, p53 is well known to bind consensus target sequences in linear B-DNA. Recent findings indicate that p53 binds with higher affinity to target sequences that form cruciform DNA structure. Moreover, p53 binds very tightly to non-B DNA structures and local DNA structures are increasingly recognized to influence the activity of wild-type and mutant p53. Apart from cruciform structures, p53 binds to quadruplex DNA, triplex DNA, DNA loops, bulged DNA and hemicatenane DNA. In this review, we describe local DNA structures and summarize information about interactions of p53 with these structural DNA motifs. These recent data provide important insights into the complexity of the p53 pathway and the functional consequences of wild-type and mutant p53 activation in normal and tumor cells.
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“p53 also binds a set of noncanonical DNAs, such as cruciforms, left-handed DNA (Z-DNA), quadruplex and triplex DNA.293,294”
From Targeting p53 pathways: mechanisms, structures, and advances in therapy (2023) · cites this paper as [293]
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Crystal Structure of a p53 Tumor Suppressor-DNA Complex: Understanding Tumorigenic Mutations
Cho, Y., Gorina, S., Jeffrey, P. D., & Pavletich, N. P. (1994) · Science · doi:10.1126/science.8023157 · Cited by 2,551 · cited 1×
“The core domain of the p53 protein is mainly responsible for DNA target sequence interactions [77,78], but C-terminal modification is mandatory for effective binding of the full-length protein to the target sequence [79].”
BackgroundMammalian Telomeres End in a Large Duplex Loop
Griffith, J. D., Comeau, L., Rosenfield, S., Stansel, R. M., Bianchi, A., Moss, H., & de Lange, T. (1999) · Cell · doi:10.1016/s0092-8674(00)80760-6 · Cited by 2,447
Definition of a consensus binding site for p53
El-Deiry, W. S., Kern, S. E., Pietenpol, J. A., Kinzler, K. W., & Vogelstein, B. (1992) · Nature Genetics · doi:10.1038/ng0492-45 · Cited by 1,985
Petitjean, A., Mathe, E., Kato, S., Ishioka, C., Tavtigian, S. V., Hainaut, P., & Olivier, M. (2007) · Human Mutation · doi:10.1002/humu.20495 · Cited by 1,598 · cited 1×
“The vertical bars indicate the relative missense-mutation frequency in human cancer for each residue (Tp53 Mutation Database [69].”
BackgroundA Global Map of p53 Transcription-Factor Binding Sites in the Human Genome
Wei, C.-L., Wu, Q., Vega, V. B., Chiu, K. P., Ng, P., Zhang, T., Shahab, A., Yong, H. C., Fu, Y., Weng, Z., et al. (2006) · Cell · doi:10.1016/j.cell.2005.10.043 · Cited by 1,141
An RNA G-quadruplex in the 5′ UTR of the NRAS proto-oncogene modulates translation
Kumari, S., Bugaut, A., Huppert, J. L., & Balasubramanian, S. (2007) · Nature Chemical Biology · doi:10.1038/nchembio864 · Cited by 822
The expanding universe of p53 targets
Menendez, D., Inga, A., & Resnick, M. A. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2730 · Cited by 568
Mutant p53 Cooperates with ETS and Selectively Up-regulates Human MDR1 Not MRP1
Sampath, J., Sun, D., Kidd, V. J., Grenet, J., Gandhi, A., Shapiro, L. H., Wang, Q., Zambetti, G. P., & Schuetz, J. D. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m103429200 · Cited by 244
Noncanonical DNA Motifs as Transactivation Targets by Wild Type and Mutant p53
Jordan, J. J., Menendez, D., Inga, A., Nourredine, M., Bell, D., & Resnick, M. A. (2008) · PLoS Genetics · doi:10.1371/journal.pgen.1000104 · Cited by 103
High-Affinity Binding of Tumor-Suppressor Protein p53 and HMGB1 to Hemicatenated DNA Loops
Štros, M., Muselíková-Polanská, E., Pospíšilová, Š., & Strauss, F. (2004) · Biochemistry · doi:10.1021/bi049928k · Cited by 81
Research works printed but not linked: 144
- Goh, 2011, The role of mutant p53 in human cancer, J. Pathol., 223, 116, 10.1002/path.2784 · DOI · Paper page
- Meek, 2015, Regulation of the p53 response and its relationship to cancer, Biochem. J., 469, 325, 10.1042/BJ20150517 · DOI · Paper page
- Vousden, 2007, p53 in health and disease, Nat. Rev. Mol. Cell Biol., 8, 275, 10.1038/nrm2147 · DOI · Paper page
- Lohrum, 1999, Regulation and activation of p53 and its family members, Cell Death Differ., 6, 1162, 10.1038/sj.cdd.4400625 · DOI
- Zhao, 2009, Cellular adaptation to hypoxia and p53 transcription regulation, J. Zhejiang Univ. Sci. B, 10, 404, 10.1631/jzus.B0820293 · DOI
- Itoh, 2016, Activation of p53 facilitates the target search in DNA by enhancing the target recognition probability, J. Mol. Biol., 428, 2916, 10.1016/j.jmb.2016.06.001 · DOI
- Watson, 1953, Molecular structure of nucleic acids: A structure for deoxyribose nucleic acid, Nature, 171, 737, 10.1038/171737a0 · DOI · Paper page
- Choi, 2011, Conformational changes of non-B DNA, Chem. Soc. Rev., 40, 5893, 10.1039/c1cs15153c · DOI · Paper page
- Palecek, 1991, Local supercoil-stabilized DNA structures, Crit. Rev. Biochem. Mol. Biol., 26, 151, 10.3109/10409239109081126 · DOI · Paper page
- Zlatanova, 1994, Unusual DNA structures, chromatin and transcription, Bioessays, 16, 59, 10.1002/bies.950160110 · DOI
- Wells, 2007, Non-B DNA conformations, mutagenesis and disease, Trends Biochem. Sci., 32, 271, 10.1016/j.tibs.2007.04.003 · DOI · Paper page
- Cer, R.Z., Bruce, K.H., Donohue, D.E., Temiz, N.A., Mudunuri, U.S., Yi, M., Volfovsky, N., Bacolla, A., Luke, B.T., and Collins, J.R. (2012). Searching for non-B DNA-forming motifs using nBMST (non-B DNA motif search tool). Current Protocols in Human Genetics, John Wiley Sons, Inc. · DOI
- Chasovskikh, 2005, DNA transitions induced by binding of PARP-1 to cruciform structures in supercoiled plasmids, Cytometry A, 68, 21, 10.1002/cyto.a.20187 · doi:10.1002/cyto.a.20187
- Limanskaia, 2009, Species-specific detection of Mycobacterium tuberculosis complex, Probl. Tuberk. Bolezn. Legk., 10, 49
- Mikheikin, 2006, Effect of DNA supercoiling on the geometry of holliday junctions, Biochemistry, 45, 12998, 10.1021/bi061002k · doi:10.1021/bi061002k
- Pearson, 1996, Inverted repeats, stem-loops, and cruciforms: Significance for initiation of DNA replication, J. Cell. Biochem., 63, 1, 10.1002/(SICI)1097-4644(199610)63:1<1::AID-JCB1>3.0.CO;2-3 · DOI
- Werbowy, 2009, Characterization of a cryptic plasmid pSFKW33 from Shewanella sp. 33B, Plasmid, 62, 44, 10.1016/j.plasmid.2009.03.003 · doi:10.1016/j.plasmid.2009.03.003
- Brazda, 2016, Palindrome analyser—A new web-based server for predicting and evaluating inverted repeats in nucleotide sequences, Biochem. Biophys. Res. Commun., 478, 1739, 10.1016/j.bbrc.2016.09.015 · DOI
- Cer, 2011, Non-B DB: A database of predicted non-B DNA-forming motifs in mammalian genomes, Nucleic Acids Res., 39, D383, 10.1093/nar/gkq1170 · DOI
- Aranda, 1997, Analysis of the structure of a natural alternating d(TA)n sequence in yeast chromatin, Yeast, 13, 313, 10.1002/(SICI)1097-0061(19970330)13:4<313::AID-YEA93>3.0.CO;2-8 · doi:10.1002/(sici)1097-0061(19970330)13:4<313::aid-yea93>3.0.co;2-8
- Kurahashi, 2004, Cruciform DNA structure underlies the etiology for palindrome-mediated human chromosomal translocations, J. Biol. Chem., 279, 35377, 10.1074/jbc.M400354200 · doi:10.1074/jbc.m400354200
- Lyubchenko, 2004, DNA structure and dynamics: An atomic force microscopy study, Cell Biochem. Biophys., 41, 75, 10.1385/CBB:41:1:075 · DOI
- Shlyakhtenko, 1998, Structure and dynamics of supercoil-stabilized DNA cruciforms, J. Mol. Biol., 280, 61, 10.1006/jmbi.1998.1855 · DOI · Paper page
- Shlyakhtenko, 2000, A cruciform structural transition provides a molecular switch for chromosome structure and dynamics, J. Mol. Biol., 296, 1169, 10.1006/jmbi.2000.3542 · DOI
- Panayotatos, 1987, A native cruciform DNA structure probed in bacteria by recombinant T7 endonuclease, J. Biol. Chem., 262, 11364, 10.1016/S0021-9258(18)60968-8 · doi:10.1016/s0021-9258(18)60968-8
- Yamaguchi, 1984, The replication origin of pSC101: The nucleotide sequence and replication functions of the ori region, Gene, 29, 211, 10.1016/0378-1119(84)90181-1 · doi:10.1016/0378-1119(84)90181-1
- Brazda, V., Laister, R.C., Jagelska, E.B., and Arrowsmith, C. (2011). Cruciform structures are a common DNA feature important for regulating biological processes. BMC Mol. Biol., 12. · DOI
- Manelyte, L., Strohner, R., Gross, T., and Langst, G. (2014). Chromatin targeting signals, nucleosome positioning mechanism and non-coding RNA-mediated regulation of the chromatin remodeling complex NoRC. PLoS Genet., 10. · DOI
- Yahyaoui, W., Callejo, M., Price, G.B., and Zannis-Hadjopoulos, M. (2007). Deletion of the cruciform binding domain in CBP/14-3-3 displays reduced origin binding and initiation of DNA replication in budding yeast. BMC Mol. Biol., 8. · DOI
- Muller, 2002, Analysis of hypermethylation in the RPS element suggests a signal function for short inverted repeats in de novo methylation, Plant Mol. Biol., 48, 383, 10.1023/A:1014091131490 · doi:10.1023/a:1014091131490
- Gentry, 2016, A structural bisulfite assay to identify DNA cruciforms, Mol. Plant, 9, 1328, 10.1016/j.molp.2016.06.003 · doi:10.1016/j.molp.2016.06.003
- Mirkin, 1995, Triplex DNA structures, Annu. Rev. Biochem., 64, 65, 10.1146/annurev.bi.64.070195.000433 · DOI · Paper page
- Mukherjee, 2011, Triplex technology in studies of DNA damage, DNA repair, and mutagenesis, Biochimie, 93, 1197, 10.1016/j.biochi.2011.04.001 · DOI
- Lee, 2010, DNA complexes containing joined triplex and duplex motifs: Melting behavior of intramolecular and bimolecular complexes with similar sequences, J. Phys. Chem. B, 114, 541, 10.1021/jp9084074 · DOI
- Bacolla, 2009, Non-B DNA conformations as determinants of mutagenesis and human disease, Mol. Carcinog., 48, 273, 10.1002/mc.20507 · DOI
- Schroth, 1995, Occurrence of potential cruciform and H-DNA forming sequences in genomic DNA, Nucleic Acids Res., 23, 1977, 10.1093/nar/23.11.1977 · DOI
- Wu, 2007, High-affinity triplex-forming oligonucleotide target sequences in mammalian genomes, Mol. Carcinog., 46, 15, 10.1002/mc.20261 · doi:10.1002/mc.20261
- Bacolla, 2006, Long homopurine·homopyrimidine sequences are characteristic of genes expressed in brain and the pseudoautosomal region, Nucleic Acids Res., 34, 2663, 10.1093/nar/gkl354 · DOI
- Gorab, 2009, Potential sites of triple-helical nucleic acid formation in chromosomes of Rhynchosciara (Diptera: Sciaridae) and Drosophila melanogaster, Chromosome Res., 17, 821, 10.1007/s10577-009-9075-5 · doi:10.1007/s10577-009-9075-5
- Hoyne, 2002, Functional studies of potential intrastrand triplex elements in the Escherichia coli genome, J. Mol. Biol., 318, 373, 10.1016/S0022-2836(02)00041-4 · doi:10.1016/s0022-2836(02)00041-4
- Krasilnikova, 2004, Replication stalling at Friedreich’s ataxia (GAA)n repeats in vivo, Mol. Cell. Biol., 24, 2286, 10.1128/MCB.24.6.2286-2295.2004 · DOI · Paper page
- Mariappan, 1999, The high-resolution structure of the triplex formed by the GAA/TTC triplet repeat associated with Friedreich’s ataxia, J. Mol. Biol., 285, 2035, 10.1006/jmbi.1998.2435 · DOI
- Rajeswari, 2012, DNA triplex structures in neurodegenerative disorder, Friedreich’s ataxia, J. Biosci., 37, 519, 10.1007/s12038-012-9219-1 · DOI
- Jain, 2002, Formation and thermodynamic stability of intermolecular (R*R·Y) DNA triplex in GAA/TTC repeats associated with Freidreich’s ataxia, J. Biomol. Struct. Dyn., 19, 691, 10.1080/07391102.2002.10506775 · doi:10.1080/07391102.2002.10506775
- Bowater, 2001, The intrinsically unstable life of DNA triplet repeats associated with human hereditary disorders, Prog. Nucleic Acid. Res. Mol. Biol., 66, 159, 10.1016/S0079-6603(00)66029-4 · DOI
- Singh, 2015, Role of long purine stretches in controlling the expression of genes associated with neurological disorders, Gene, 572, 175, 10.1016/j.gene.2015.07.007 · DOI
- Bochman, 2012, DNA secondary structures: Stability and function of G-quadruplex structures, Nat. Rev. Genet., 13, 770, 10.1038/nrg3296 · DOI · Paper page
- Neidle, 2008, Quadruplex DNA crystal structures and drug design, Biochimie, 90, 1184, 10.1016/j.biochi.2008.03.003 · DOI
- Gellert, 1962, Helix formation by guanylic acid, Proc. Natl. Acad. Sci. USA, 48, 2013, 10.1073/pnas.48.12.2013 · DOI · Paper page
- Wang, 1993, Solution structure of the human telomeric repeat d[AG3(T2AG3)3] G-tetraplex, Structure, 1, 263, 10.1016/0969-2126(93)90015-9 · DOI · Paper page
- Huppert, 2007, G-quadruplexes in promoters throughout the human genome, Nucleic Acids Res., 35, 406, 10.1093/nar/gkl1057 · DOI · Paper page
- Kikin, 2006, QGRS Mapper: A web-based server for predicting G-quadruplexes in nucleotide sequences, Nucleic Acids Res., 34, W676, 10.1093/nar/gkl253 · DOI · Paper page
- Scaria, 2006, Quadfinder: Server for identification and analysis of quadruplex-forming motifs in nucleotide sequences, Nucleic Acids Res., 34, W683, 10.1093/nar/gkl299 · doi:10.1093/nar/gkl299
- Schaffitzel, 2001, In vitro generated antibodies specific for telomeric guanine-quadruplex DNA react with Stylonychia lemnae macronuclei, Proc. Natl. Acad. Sci. USA, 98, 8572, 10.1073/pnas.141229498 · DOI · Paper page
- Yang, 2009, Verification of specific G-quadruplex structure by using a novel cyanine dye supramolecular assembly: I. recognizing mixed G-quadruplex in human telomeres, Chem. Commun., 9, 1103, 10.1039/b820101c · DOI
- Gros, 2008, DNA and RNA quadruplex ligands, Nucleic Acids Symp. Ser., 52, 7, 10.1093/nass/nrn004 · DOI
- Eddy, 2006, Gene function correlates with potential for G4 DNA formation in the human genome, Nucleic Acids Res., 34, 3887, 10.1093/nar/gkl529 · DOI · Paper page
- Eddy, 2009, Selection for the G4 DNA motif at the 5’ end of human genes, Mol. Carcinog., 48, 319, 10.1002/mc.20496 · DOI
- Stansel, 2001, T-loop assembly in vitro involves binding of TRF2 near the 3′ telomeric overhang, EMBO J., 20, 5532, 10.1093/emboj/20.19.5532 · DOI · Paper page
- Murti, 1999, Telomeres of polytene chromosomes in a ciliated protozoan terminate in duplex DNA loops, Proc. Natl. Acad. Sci. USA, 96, 14436, 10.1073/pnas.96.25.14436 · DOI
- Cross, 2001, T-loops at trypanosome telomeres, EMBO J., 20, 579, 10.1093/emboj/20.3.579 · DOI · Paper page
- Levine, 1997, p53, the cellular gatekeeper for growth and division, Cell, 88, 323, 10.1016/S0092-8674(00)81871-1 · DOI · Paper page
- Yang, 2007, In silico analysis of p53 using the p53 knowledgebase: Mutations, polymorphisms, microRNAs and pathways, In Silico Biol., 7, 61, 10.3233/ISB-00275 · doi:10.3233/isb-00275
- Joerger, 2008, Structural biology of the tumor suppressor p53, Annu. Rev. Biochem., 77, 557, 10.1146/annurev.biochem.77.060806.091238 · DOI · Paper page
- Joerger, 2010, The tumor suppressor p53: From structures to drug discovery, Cold Spring Harb. Perspect. Biol., 2, a000919, 10.1101/cshperspect.a000919 · DOI · Paper page
- Okorokov, 2009, Structural biology of the p53 tumour suppressor, Curr. Opin. Struct. Biol., 19, 197, 10.1016/j.sbi.2009.02.003 · DOI
- Qian, 2002, Groups of p53 target genes involved in specific p53 downstream effects cluster into different classes of DNA binding sites, Oncogene, 21, 7901, 10.1038/sj.onc.1205974 · DOI
- Balagurumoorthy, 1995, Four p53 DNA-binding domain peptides bind natural p53-response elements and bend the DNA, Proc. Natl. Acad. Sci. USA, 92, 8591, 10.1073/pnas.92.19.8591 · DOI
- Weinberg, 2005, Comparative binding of p53 to its promoter and DNA recognition elements, J. Mol. Biol., 348, 589, 10.1016/j.jmb.2005.03.014 · DOI · Paper page
- Kim, 1997, DNA-conformation is an important determinant of sequence-specific DNA binding by tumor suppressor p53, Oncogene, 15, 857, 10.1038/sj.onc.1201412 · DOI
- Inga, 2002, Differential transactivation by the p53 transcription factor is highly dependent on p53 level and promoter target sequence, Mol. Cell. Biol., 22, 8612, 10.1128/MCB.22.24.8612-8625.2002 · DOI · Paper page
- Ma, 2007, Sequence analysis of p53 response-elements suggests multiple binding modes of the p53 tetramer to DNA targets, Nucleic Acids Res., 35, 2986, 10.1093/nar/gkm192 · DOI
- Chen, 2010, Crystal structure of the p53 core domain bound to a full consensus site as a self-assembled tetramer, Structure, 18, 246, 10.1016/j.str.2009.11.011 · DOI · Paper page
- Gohler, 2002, Specific interaction of p53 with target binding sites is determined by DNA conformation and is regulated by the C-terminal domain, J. Biol. Chem., 277, 41192, 10.1074/jbc.M202344200 · DOI
- McKinney, 2002, Efficient specific DNA binding by p53 requires both its central and C-terminal domains as revealed by studies with high-mobility group 1 protein, Mol. Cell. Biol., 22, 6797, 10.1128/MCB.22.19.6797-6808.2002 · DOI
- McKinney, 2004, p53 linear diffusion along DNA requires its C terminus, Mol. Cell, 16, 413, 10.1016/j.molcel.2004.09.032 · DOI · Paper page
- Brazda, 2006, Searching for target sequences by p53 protein is influenced by DNA length, Biochem. Biophys. Res. Commun., 341, 470, 10.1016/j.bbrc.2005.12.202 · doi:10.1016/j.bbrc.2005.12.202
- Murata, 2015, One-dimensional sliding of p53 along DNA is accelerated in the presence of Ca2+ or Mg2+ at millimolar concentrations, J. Mol. Biol., 427, 2663, 10.1016/j.jmb.2015.06.016 · DOI
- Tafvizi, 2011, A single-molecule characterization of p53 search on DNA, Proc. Natl. Acad. Sci. USA, 108, 563, 10.1073/pnas.1016020107 · DOI · Paper page
- Leith, 2012, Sequence-dependent sliding kinetics of p53, Proc. Natl. Acad. Sci. USA, 109, 16552, 10.1073/pnas.1120452109 · DOI
- Terakawa, 2012, p53 searches on DNA by rotation-uncoupled sliding at C-terminal tails and restricted hopping of core domains, J. Am. Chem. Soc., 134, 14555, 10.1021/ja305369u · DOI · Paper page
- Veprintsev, 2008, Algorithm for prediction of tumour suppressor p53 affinity for binding sites in DNA, Nucleic Acids Res., 36, 1589, 10.1093/nar/gkm1040 · DOI
- Wang, 2009, Redefining the p53 response element, Proc. Natl. Acad. Sci. USA, 106, 14373, 10.1073/pnas.0903284106 · DOI
- Allen, 2014, Global analysis of p53-regulated transcription identifies its direct targets and unexpected regulatory mechanisms, eLife, 3, e02200, 10.7554/eLife.02200 · DOI · Paper page
- Chang, 2014, A comprehensive and high-resolution genome-wide response of p53 to stress, Cell Rep., 8, 514, 10.1016/j.celrep.2014.06.030 · DOI
- Nagaich, 1997, DNA bending is essential for the site-specific recognition of DNA response elements by the DNA binding domain of the tumor suppressor protein p53, J. Biol. Chem., 272, 14842, 10.1074/jbc.272.23.14842 · DOI
- Nagaich, 1999, p53-induced DNA bending and twisting: p53 tetramer binds on the outer side of a DNA loop and increases DNA twisting, Proc. Natl. Acad. Sci. USA, 96, 1875, 10.1073/pnas.96.5.1875 · DOI
- Jordan, 2012, Low-level p53 expression changes transactivation rules and reveals superactivating sequences, Proc. Natl. Acad. Sci. USA, 109, 14387, 10.1073/pnas.1205971109 · DOI
- Petty, 2011, An induced fit mechanism regulates p53 DNA binding kinetics to confer sequence specificity, EMBO J., 30, 2167, 10.1038/emboj.2011.127 · DOI · Paper page
- Tubbs, 2011, p53 conformational switching for selectivity may reveal a general solution for specific DNA binding, EMBO J., 30, 2099, 10.1038/emboj.2011.133 · doi:10.1038/emboj.2011.133
- Demir, O., Ieong, P.U., and Amaro, R.E. (2016). Full-length p53 tetramer bound to DNA and its quaternary dynamics. Oncogene. · DOI · Paper page
- Niederweis, 1993, Electrophoretic analysis of protein-induced DNA bending and twist changes, Electrophoresis, 14, 693, 10.1002/elps.11501401110 · doi:10.1002/elps.11501401110
- Palecek, 1997, Tumor suppressor protein p53 binds preferentially to supercoiled DNA, Oncogene, 15, 2201, 10.1038/sj.onc.1201398 · DOI
- Brazdova, M., Navratilova, L., Tichy, V., Nemcova, K., Lexa, M., Hrstka, R., Pecinka, P., Adamik, M., Vojtesek, B., and Palecek, E. (2013). Preferential binding of hot spot mutant p53 proteins to supercoiled DNA in vitro and in cells. PLoS ONE, 8. · DOI
- Adamik, 2016, p53 binds human telomeric G-quadruplex in vitro, Biochimie, 128, 83, 10.1016/j.biochi.2016.07.004 · doi:10.1016/j.biochi.2016.07.004
- Kim, 1999, Influence of promoter DNA topology on sequence-specific DNA binding and transactivation by tumor suppressor p53, Oncogene, 18, 7310, 10.1038/sj.onc.1203139 · DOI
- Jagelska, 2008, DNA topology influences p53 sequence-specific DNA binding through structural transitions within the target sites, Biochem. J., 412, 57, 10.1042/BJ20071648 · DOI
- Palecek, 2004, Enhancement of p53 sequence-specific binding by DNA supercoiling, Oncogene, 23, 2119, 10.1038/sj.onc.1207324 · DOI
- Jagelska, 2010, The potential of the cruciform structure formation as an important factor influencing p53 sequence-specific binding to natural DNA targets, Biochem. Biophys. Res. Commun., 391, 1409, 10.1016/j.bbrc.2009.12.076 · DOI
- Coufal, 2013, Preferential binding of p53 tumor suppressor to p21 promoter sites that contain inverted repeats capable of forming cruciform structure, Biochem. Biophys. Res. Commun., 441, 83, 10.1016/j.bbrc.2013.10.015 · DOI
- Battistin, 2017, The structure formed by inverted repeats in p53 response elements determines the transactivation activity of p53 protein, Biochem. Biophys. Res. Commun., 483, 516, 10.1016/j.bbrc.2016.12.113 · DOI
- Degtyareva, 2001, Analysis of the binding of p53 to DNAs containing mismatched and bulged bases, J. Biol. Chem., 276, 8778, 10.1074/jbc.M006795200 · DOI
- Kim, 2003, The complex interactions of p53 with target DNA: We learn as we go, Biochem. Cell Biol., 81, 141, 10.1139/o03-046 · DOI
- Subramanian, 2005, p53 Monitors replication fork regression by binding to “chickenfoot” intermediates, J. Biol. Chem., 280, 42568, 10.1074/jbc.M506348200 · DOI
- Stansel, 2002, p53 binds telomeric single strand overhangs and T-loop junctions in vitro, J. Biol. Chem., 277, 11625, 10.1074/jbc.C100764200 · DOI
- Brazda, 2000, Specific modulation of p53 binding to consensus sequence within supercoiled DNA by monoclonal antibodies, Biochem. Biophys. Res. Commun., 267, 934, 10.1006/bbrc.1999.2056 · DOI
- Palecek, 2001, Binding of p53 and its core domain to supercoiled DNA, Eur. J. Biochem., 268, 573, 10.1046/j.1432-1327.2001.01898.x · DOI
- Lee, 1995, p53 and Its 14 kDa C-terminal domain recognize primary DNA-damage in the form of insertion deletion mismatches, Cell, 81, 1013, 10.1016/S0092-8674(05)80006-6 · DOI · Paper page
- Cobb, 2013, Sequence-specific and DNA structure-dependent interactions of Escherichia coli MutS and human p53 with DNA, Anal. Biochem., 442, 51, 10.1016/j.ab.2013.07.033 · DOI
- Lee, 1997, Human p53 binds Holliday junctions strongly and facilitates their cleavage, J. Biol. Chem., 272, 7532, 10.1074/jbc.272.11.7532 · DOI
- Picksley, 1992, The conformational change of a murine temperature-sensitive p53 protein is independent of a change in phosphorylation status, Oncogene, 7, 1649
- Mazur, 1999, Preferential binding of tumor suppressor p53 to positively or negatively supercoiled DNA involves the C-terminal domain, J. Mol. Biol., 292, 241, 10.1006/jmbi.1999.3064 · DOI
- Pivonkova, 2010, Selective binding of tumor suppressor p53 protein to topologically constrained DNA: Modulation by intercalative drugs, Biochem. Biophys. Res. Commun., 393, 894, 10.1016/j.bbrc.2010.02.120 · DOI
- Jett, 2000, Scanning force microscopy of the complexes of p53 core domain with supercoiled DNA, J. Mol. Biol., 299, 585, 10.1006/jmbi.2000.3759 · DOI
- Cherny, 1999, DNA bending due to specific p53 and p53 core domain-DNA interactions visualized by electron microscopy, J. Mol. Biol., 294, 1015, 10.1006/jmbi.1999.3299 · DOI
- Saramaki, 2006, Regulation of the human p21(waf1/cip1) gene promoter via multiple binding sites for p53 and the vitamin D3 receptor, Nucleic Acids Res., 34, 543, 10.1093/nar/gkj460 · DOI
- Gaillard, C., and Strauss, F. (2000). High affinity binding of proteins HMG1 and HMG2 to semicatenated DNA loops. BMC Mol. Biol., 1. · DOI
- Lee, 2013, Regulation of hypoxia-iinducible factor 1α (HIF-1α) by lysophosphatidic acid is dependent on interplay between p53 and Kruppel-like factor 5, J. Biol. Chem., 288, 25244, 10.1074/jbc.M113.489708 · DOI
- Kasparkova, 2001, Different recognition of DNA modified by aatitumor cisplatin and its clinically ineffective trans isomer by tumor suppressor protein p53, J. Biol. Chem., 276, 16064, 10.1074/jbc.M101224200 · DOI
- Bakalkin, 1994, p53 binds single-stranded DNA ends and catalyzes DNA renaturation and strand transfer, Proc. Natl. Acad. Sci. USA, 91, 413, 10.1073/pnas.91.1.413 · DOI · Paper page
- Thomas, 1995, Suppression of c-myc oncogene expression by a polyamine-complexed triplex forming oligonucleotide in MCF-7 breast cancer cells, Nucleic Acids Res., 23, 3594, 10.1093/nar/23.17.3594 · DOI
- Brazdova, M., Tichy, V., Helma, R., Bazantova, P., Polaskova, A., Krejci, A., Petr, M., Navratilova, L., Ticha, O., and Nejedly, K. (2016). p53 specifically binds triplex DNA in vitro and in cells. PLoS ONE, 11. · DOI
- Rhodes, 2015, G-quadruplexes and their regulatory roles in biology, Nucleic Acids Res., 43, 8627, 10.1093/nar/gkv862 · DOI · Paper page
- Haronikova, L., Coufal, J., Kejnovska, I., Jagelska, E.B., Fojta, M., Dvorakova, P., Muller, P., Vojtesek, B., and Brazda, V. (2016). IFI16 preferentially binds to DNA with quadruplex structure and enhances DNA quadruplex formation. PLoS ONE, 11. · DOI
- Gohler, 2005, Mutant p53 proteins bind DNA in a DNA structure-selective mode, Nucleic Acids Res., 33, 1087, 10.1093/nar/gki252 · DOI
- Brazda, 2006, Restoring wild-type conformation and DNA-binding activity of mutant p53 is insufficient for restoration of transcriptional activity, Biochem. Biophys. Res. Commun., 351, 499, 10.1016/j.bbrc.2006.10.065 · DOI
- Quante, 2012, Mutant p53 is a transcriptional co-factor that binds to G-rich regulatory regions of active genes and generates transcriptional plasticity, Cell Cycle, 11, 3290, 10.4161/cc.21646 · DOI
- Brazdova, 2009, Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences, Nucleic Acids Res., 37, 1486, 10.1093/nar/gkn1085 · DOI
- Chicas, 2000, Mutant p53 forms a complex with Sp1 on HIV-LTR DNA, Biochem. Biophys. Res. Commun., 279, 383, 10.1006/bbrc.2000.3965 · DOI
- Petr, 2016, Wild-type p53 binds to MYC promoter G-quadruplex, Biosci. Rep., 36, e00397, 10.1042/BSR20160232 · DOI
- Walter, 2005, Tumor suppressor p53 binds with high affinity to CTG·CAG trinucleotide repeats and induces topological alterations in mismatched duplexes, J. Biol. Chem., 280, 42497, 10.1074/jbc.M507038200 · DOI
- Kamada, 2016, Tetramer formation of tumor suppressor protein p53: Structure, function, and applications, Biopolymers, 106, 598, 10.1002/bip.22772 · DOI · Paper page
- Chene, 2001, The role of tetramerization in p53 function, Oncogene, 20, 2611, 10.1038/sj.onc.1204373 · DOI · Paper page
- Oren, 2010, Mutant p53 gain-of-function in cancer, Cold Spring Harb. Perspect. Biol., 2, a001107, 10.1101/cshperspect.a001107 · DOI · Paper page
- Strano, 2007, Mutant p53 proteins: Between loss and gain of function, Head Neck, 29, 488, 10.1002/hed.20531 · DOI
- Noy, 2016, Protein/DNA interactions in complex DNA topologies: Expect the unexpected, Biophys. Rev., 8, 233, 10.1007/s12551-016-0208-8 · DOI
- Brazda, 2014, DNA and RNA quadruplex-binding proteins, Int. J. Mol. Sci., 15, 17493, 10.3390/ijms151017493 · DOI
- Kim, 2006, The versatile interactions of p53 with DNA: When flexibility serves specificity, Cell Death Differ., 13, 885, 10.1038/sj.cdd.4401909 · DOI
- Deppert, 1996, Binding of MAR-DNA elements by mutant p53: Possible implications for its oncogenic functions, J. Cell. Biochem., 62, 172, 10.1002/(SICI)1097-4644(199608)62:2<172::AID-JCB5>3.0.CO;2-P · doi:10.1002/(sici)1097-4644(199608)62:2<172::aid-jcb5>3.0.co;2-p
- Will, 1998, Specific interaction of mutant p53 with regions of matrix attachment region DNA elements (MARs) with a high potential for base-unpairing, Proc. Natl. Acad. Sci. USA, 95, 13681, 10.1073/pnas.95.23.13681 · DOI
- Laptenko, 2016, The tail that wags the dog: How the disordered C-terminal domain controls the transcriptional activities of the p53 tumor-suppressor protein, Trends Biochem. Sci., 41, 1022, 10.1016/j.tibs.2016.08.011 · DOI · Paper page
- Kim, 2004, Transcriptional activities of mutant p53: When mutations are more than a loss, J. Cell. Biochem., 93, 878, 10.1002/jcb.20271 · DOI
- Tutton, 2016, Subtelomeric p53 binding prevents accumulation of DNA damage at human telomeres, EMBO J., 35, 193, 10.15252/embj.201490880 · DOI
- Bieging, 2013, Global genomic profiling reveals an extensive p53-regulated autophagy program contributing to key p53 responses, Genes Dev., 27, 1016, 10.1101/gad.212282.112 · DOI · Paper page
Cited by
Targeting p53 pathways: mechanisms, structures, and advances in therapy
Wang, H., Guo, M., Wei, H., & Chen, Y. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01347-1 · Cited by 1,016
Metadata
- Authors
- Brázda, V., & Coufal, J.
- Affiliations
- Institute of Biophysics, Academy of Sciences of the Czech Republic v.v.i., Královopolská 135, 612 65 Brno, Czech Republic
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2017-02-10
- Volume
- 18
- Issue
- 2
- Pages
- 375
- ISSN
- 1422-0067
- Cited by
- 38
- References
- 10
- Language
- en
- Update notices
- correction (2017-02-10)
- Funders
- Grantová Agentura České Republiky (15-21855S)
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- This page
- CoChat. (2026). Citation check: Recognition of Local DNA Structures by p53 Protein. https://app.cochat.ai/papers/10.3390/ijms18020375
- The paper
- Brázda, V., & Coufal, J. (2017). Recognition of Local DNA Structures by p53 Protein. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms18020375
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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