ArticleMolecular and cellular biology2000
The N-terminal domain of p73 interacts with the CH1 domain of p300/CREB binding protein and mediates transcriptional activation and apoptosis.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 97 citations in OpenAlex.
- Distinct interactors define the p63 transcriptional signature in epithelial development or cancer.The Biochemical journal · 2022Article
- Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Targeting Post-Translational Modifications of the p73 Protein: A Promising Therapeutic Strategy for Tumors.Cancers · 2021Review
- Review
- Characterization of the new human pleomorphic undifferentiated sarcoma TP53-null cell line mfh-val2.Cytotechnology · 2017Article
- FGF8, c-Abl and p300 participate in a pathway that controls stability and function of the ΔNp63α protein.Human molecular genetics · 2015Article
- Interplay between TAp73 Protein and Selected Activator Protein-1 (AP-1) Family Members Promotes AP-1 Target Gene Activation and Cellular Growth.The Journal of biological chemistry · 2015Article
- Ribosomal proteins L11 and L5 activate TAp73 by overcoming MDM2 inhibition.Cell death and differentiation · 2015Article
- p53 Family and Cellular Stress Responses in Cancer.Frontiers in oncology · 2014Review
- Lysine-specific modifications of p53: a matter of life and death?Oncotarget · 2013Review
- Article
- Regulation of p73 activity by post-translational modifications.Cell death & disease · 2012Review
- Direct activation of forkhead box O3 by tumor suppressors p53 and p73 is disrupted during liver regeneration in mice.Hepatology (Baltimore, Md.) · 2010Article
- NIR, an inhibitor of histone acetyltransferases, regulates transcription factor TAp63 and is controlled by the cell cycle.Nucleic acids research · 2010Article
- p73-Binding Partners and Their Functional Significance.International journal of proteomics · 2010Article
- Molecular basis of the interactions between the p73 N terminus and p300: effects on transactivation and modulation by phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- The p53 family and programmed cell death.Oncogene · 2008Review
- A new coactivator function for Zac1's C2H2 zinc finger DNA-binding domain in selectively controlling PCAF activity.Molecular and cellular biology · 2008Article
- Cataloging and organizing p73 interactions in cell cycle arrest and apoptosis.Nucleic acids research · 2008Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The newly identified p53 homolog p73 mimics the transcriptional function of p53. We have investigated the regulation of p73's transcriptional activity by p300/CREB binding protein (CBP). p73-p300 complexes were identified in HeLa cell extracts by cofractionation and coimmunoprecipitation assays. The p73-p300 interaction was confirmed in vitro by glutathione S-transferase-protein association assays and in vivo by coimmunoprecipitating the overexpressed p300 and p73 in human p53-free small-cell lung carcinoma H1299 or osteosarcoma Saos-2 cells. The N terminus but not the N-terminal truncation of p73 bound to the CH1 domain (amino acids [aa] 350 to 450) of p300/CBP. Accordingly, this p73 N-terminal deletion was unable to activate transcription or to induce apoptosis. Overexpression of either p300 or CBP stimulated transcription mediated by p73 but not its N-terminally deleted mutant in vivo. The N-terminal fragment from aa 19 to 597, but not the truncated fragment from aa 242 to 1700 of p300, reduced p73-mediated transcription markedly. p73-dependent transcription or apoptosis was partially impaired in either p300- or CBP-deficient human breast carcinoma MCF-7 or H1299 cells, suggesting that both coactivators mediate transcription by p73 in cells. These results demonstrate that the N terminus of p73 directly interacts with the N-terminal CH1 domain of p300/CBP to activate transcription.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.