4.1 Article Data Paper

ChIP-chip data for identifying target genes and consensus binding sequences of mutant p53 in MDA-MB-468 breast cancer cells

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DATA IN BRIEF
Volume 50, Issue -, Pages -

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ELSEVIER
DOI: 10.1016/j.dib.2023.109499

Keywords

TP53; Chromatin immunoprecipitation (ChIP); DNA microarray; Transcription factor; DNA binding motif

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The tumor suppressor gene p53 acts as a transcription factor and is commonly mutated in human cancers, especially triple negative breast cancer (TNBC). Mutations in the TP53 gene mainly occur in exons 5-8, resulting in changes in the DNA-binding domain of the p53 protein. A chromatin immunoprecipitation followed by DNA microarray (ChIP-chip) experiment was performed to identify target genes and binding motifs of the mutated p53 protein.
The tumor suppressor p53 exerts its role mainly as a transcription factor. The TP53 gene, which encodes the p53 protein, is the most commonly mutated gene in human cancers, particularly triple negative breast cancer (TNBC). Variations in the TP53 gene occur mainly in exons 5-8 and result in missense mutations in the DNA-binding domain of the p53 protein that alter DNA binding specificity. To identify the target genes of mutant p53, we performed chromatin immunoprecipitation followed by DNA microarray (ChIP-chip). Briefly, the TNBC cell line MDA-MB-468 containing the endogenous p53-R273H mutation (the arginine residue at position 273 is mutated to a histidine) was cross-linked with 1% formaldehyde and ultrasonically sheared to generate chromatin fragments in a range of 20 0 similar to 1000 bp. An aliquot of the sheared chromatin was kept as input, and the other chromatin was precipitated with a p53 monoclonal antibody. DNA was purified from the precipitated chromatin and the unprecipitated chromatin (i.e., input), amplified, and labeled with Cy5 (ChIP DNA) or Cy3 (input DNA). Cy5- and Cy3-labeled DNA samples were cohybridized with the NimbleGen Human ChIP-chip 2.1 M Deluxe Promoter Array. The raw and analyzed data are described in this article. They are useful for identifying target genes and consensus binding motifs of the p53 R273H mutant and for further clarifying the molecular mechanism underlying the oncogenic activity of the p53 mutant. (c) 2023 The Author(s). Published by Elsevier Inc.

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