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Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences

Standard

Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences. / Brázdová, Marie; Quante, Timo; Tögel, Lars; Walter, Korden; Loscher, Christine; Tichý, Vlastimil; Cincárová, Lenka; Deppert, Wolfgang; Tolstonog, Genrich V.

in: NUCLEIC ACIDS RES, Jahrgang 37, Nr. 5, 04.2009, S. 1486-500.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Brázdová, M, Quante, T, Tögel, L, Walter, K, Loscher, C, Tichý, V, Cincárová, L, Deppert, W & Tolstonog, GV 2009, 'Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences', NUCLEIC ACIDS RES, Jg. 37, Nr. 5, S. 1486-500. https://doi.org/10.1093/nar/gkn1085

APA

Brázdová, M., Quante, T., Tögel, L., Walter, K., Loscher, C., Tichý, V., Cincárová, L., Deppert, W., & Tolstonog, G. V. (2009). Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences. NUCLEIC ACIDS RES, 37(5), 1486-500. https://doi.org/10.1093/nar/gkn1085

Vancouver

Brázdová M, Quante T, Tögel L, Walter K, Loscher C, Tichý V et al. Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences. NUCLEIC ACIDS RES. 2009 Apr;37(5):1486-500. https://doi.org/10.1093/nar/gkn1085

Bibtex

@article{e29e9661bacc4536a5a1735caf94baee,
title = "Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences",
abstract = "Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53(R273H) in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53(R273H) targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin.",
keywords = "Binding Sites, Cell Line, Tumor, Chromatin, Chromatin Immunoprecipitation, DNA, Intergenic, Gene Expression Regulation, Neoplastic, Genes, p53, Genome, Human, Glioblastoma, Humans, Introns, Mutation, Missense, Sequence Analysis, DNA, Tumor Suppressor Protein p53",
author = "Marie Br{\'a}zdov{\'a} and Timo Quante and Lars T{\"o}gel and Korden Walter and Christine Loscher and Vlastimil Tich{\'y} and Lenka Cinc{\'a}rov{\'a} and Wolfgang Deppert and Tolstonog, {Genrich V}",
year = "2009",
month = apr,
doi = "10.1093/nar/gkn1085",
language = "English",
volume = "37",
pages = "1486--500",
journal = "NUCLEIC ACIDS RES",
issn = "0305-1048",
publisher = "Oxford University Press",
number = "5",

}

RIS

TY - JOUR

T1 - Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 R273H to intronic and intergenic sequences

AU - Brázdová, Marie

AU - Quante, Timo

AU - Tögel, Lars

AU - Walter, Korden

AU - Loscher, Christine

AU - Tichý, Vlastimil

AU - Cincárová, Lenka

AU - Deppert, Wolfgang

AU - Tolstonog, Genrich V

PY - 2009/4

Y1 - 2009/4

N2 - Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53(R273H) in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53(R273H) targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin.

AB - Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53(R273H) in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53(R273H) targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin.

KW - Binding Sites

KW - Cell Line, Tumor

KW - Chromatin

KW - Chromatin Immunoprecipitation

KW - DNA, Intergenic

KW - Gene Expression Regulation, Neoplastic

KW - Genes, p53

KW - Genome, Human

KW - Glioblastoma

KW - Humans

KW - Introns

KW - Mutation, Missense

KW - Sequence Analysis, DNA

KW - Tumor Suppressor Protein p53

U2 - 10.1093/nar/gkn1085

DO - 10.1093/nar/gkn1085

M3 - SCORING: Journal article

C2 - 19139068

VL - 37

SP - 1486

EP - 1500

JO - NUCLEIC ACIDS RES

JF - NUCLEIC ACIDS RES

SN - 0305-1048

IS - 5

ER -