A global map of p53 transcription-factor binding sites in the human genome.
By Chia-Lin Wei, Qiang Wu, V. Vega, K. Chiu, Patrick W. P. Ng, Tao Zhang, Atif Shahab, H. Yong, Yutao Fu, Zhiping Weng and 12 more. Cell, 2006
1,204 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/c482d33aa96ff447f2c92568f849320f890f459a
How researchers see this paper
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In Molecular Biology
- Johannes Rinn
- Howard Y. Chang
- Karen H. Vousden
- Eric S. Lander
- Carol Prives
- Aviv Regev
- Scott W. Lowe
- Maite Huarte
In Oncology
- Karen H. Vousden
- Carol Prives
- Scott W. Lowe
- Arnold J. Levine
- David P. Lane
- M. Guo
- Haolan Wang
- Yongheng Chen
Citations in the corpus
- Model-based Analysis of ChIP-Seq (MACS) (2008, background): “This implies that the λlocal is critical for ChIP-Seq studies when matching control samples are not available [5,9].”
- p53 in health and disease (2007, background): “Numerous studies, including the recently reported genome-wide ChIP analyses”
- Developmental roles of 21 Drosophila transcription factors are determined by quantitative differences in binding to an overlapping set of thousands of genomic regions (2009, result): “Our analysis contrasts with the predominant qualitative interpretation of in vivo crosslinking data by other groups studying animal regulators [32-46].”
- Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “The p53 pathway p53 is a transcription factor that is distributed in the nucleus and cytoplasm, binds specifically to DNA, and regulates a diversity of genes.(25,26) Under normal conditions, cellular p53 protein levels are very low owing to strict control by its negative regulators MDM2”
- Biological and molecular heterogeneity of breast cancers correlates with their cancer stem cell content. (2010, background): “(Wei et al., 2006) were significantly enriched (p < 0.”
- Transcriptional control of human p53-regulated genes (2008, methodology): “Wei and his colleagues have used chromatin immunoprecipitation with p53-specific antibodies to collect all of the tight binding sites for p53 in the genome of a cancer cell lin”
- Decoupling genetics, lineages, and microenvironment in IDH-mutant gliomas by single-cell RNA-seq (2017, background): “P53 targets were defined according to chromatin immunoprecipitation and presence of a binding motif (30).”
- A large intergenic non-coding RNA induced by p53 mediates global gene repression in the p53 response (2010, background): “The promoter region where p53 ChIP-PET fragments (black segments) map is enlarged (Wei et al., 2006).”
- Transcription Factors Bind Thousands of Active and Inactive Regions in the Drosophila Blastoderm (2008, background): “Consistent with in vivo crosslinking analyses of other animal transcription factors [39,42,80-84], the more highly crosslinked regions in vivo do, on average, show greater enrichment of factor recognition sequences than poorly bound or unbound regions (Figures 12B, 12C, and S7), indicating that thes”