ArticleThe Biochemical journal2005
Physical and functional interactions between members of the tumour suppressor p53 and the Sp families of transcription factors: importance for the regulation of genes involved in cell-cycle arrest and apoptosis.
Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 70 citations in OpenAlex.
- Proteasome dysfunction in T cells causes immunodeficiency via cell cycle disruption and apoptosis.International immunology · 2025Article
- Master regulator: p53's pivotal role in steering NK-cell tumor patrol.Frontiers in immunology · 2024Review
- The Ashkenazi-Centric G334R Variant ofMolecular and cellular biology · 2024Article
- Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021Review
- Aging and Protein Kinases.Advances in experimental medicine and biology · 2021Article
- Review
- Mithramycin selectively attenuates DNA-damage-induced neuronal cell death.Cell death & disease · 2020Article
- p53 Regulates the Expression of LRP1 and Apoptosis through a Stress Intensity-Dependent MicroRNA Feedback Loop.Cell reports · 2018Article
- Transcriptional Regulation by Wild-Type and Cancer-Related Mutant Forms of p53.Cold Spring Harbor perspectives in medicine · 2017Review
- The Role of the Ubiquitously Expressed Transcription Factor Sp1 in Tissue-specific Transcriptional Regulation and in Disease.The Yale journal of biology and medicine · 2016Review
- A/T gap tolerance in the core sequence and flanking sequence requirements of non-canonical p53 response elements.Journal of biochemistry · 2016Article
- Oncogenic Intra-p53 Family Member Interactions in Human Cancers.Frontiers in oncology · 2016Review
- ∆Np73 is capable of inducing apoptosis by co-ordinately activating several BH3-only proteins.Bioscience reports · 2015Article
- p53 cooperates with Sp1 to regulate breed-dependent expression of glucocorticoid receptor in the liver of preweaning piglets.PloS one · 2013Article
- p53 Represses transcription of RING finger LIM domain-binding protein RLIM through Sp1.PloS one · 2013Article
- SP1 plays a pivotal role for basal activity of TIGAR promoter in liver cancer cell lines.Molecular and cellular biochemistry · 2012Article
- p53 acts as a co-repressor to regulate keratin 14 expression during epidermal cell differentiation.PloS one · 2012Article
- Manganese superoxide dismutase is a p53-regulated gene that switches cancers between early and advanced stages.Cancer research · 2011Article
- p53 regulates Ki-67 promoter activity through p53- and Sp1-dependent manner in HeLa cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we have investigated mechanisms of transcriptional co-operation between proteins that belong to the tumour suppressor p53 and Sp (specificity protein) families of transcription factors. Such mechanisms may play an important role in the regulation of genes containing binding sites for both classes of transcription factors in their promoters. Two of these genes were analysed in the present study: the cyclin-dependent kinase inhibitor p21Cip1 gene and the PUMA (p53-up-regulated mediator of apoptosis) gene. We found that Sp1 and Sp3, but not Sp2, co-operate functionally with p53, p73 and p63 for the synergistic transactivation of the p21Cip1 promoter in Drosophila Schneider SL2 cells that lack endogenous Sp factors. We also found that Sp1 strongly transactivated the PUMA promoter synergistically with p53, whereas deletion of the Sp1-binding sites abolished the transactivation by p53. Using p53 mutant forms in GST (glutathione S-transferase) pull-down assays, we found that the C-terminal 101 amino acids of p53, which include the oligomerization and regulatory domains of the protein, are required for the physical interactions with Sp1 and Sp3, and that deletion of this region abolished transactivation of the p21Cip1 promoter. Utilizing truncated forms of Sp1, we established that p53 interacted with the two transactivation domains A and B, as well as the DNA-binding domain. Our findings suggest that Sp factors are essential for the cellular responses to p53 activation by genotoxic stress. Understanding in detail how members of the p53 and Sp families of transcription factors interact and work together in the p53-mediated cellular responses may open new horizons in cancer chemotherapy.
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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.