ArticleMolecular and cellular biology2003
Retinoic acid receptor alpha fusion to PML affects its transcriptional and chromatin-remodeling properties.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 33 citations in OpenAlex.
- Systems Biology for Drug Target Discovery in Acute Myeloid Leukemia.International journal of molecular sciences · 2024Article
- The phenotypic reversion of cancer: Experimental evidences on cancer reversibility through epigenetic mechanisms (Review).Oncology reports · 2024Review
- The immunomodulatory role of all-trans retinoic acid in tumor microenvironment.Clinical and experimental medicine · 2023Review
- In vivo temporal resolution of acute promyelocytic leukemia progression reveals a role ofGenes & development · 2022Article
- Emerging role of tumor cell plasticity in modifying therapeutic response.Signal transduction and targeted therapy · 2020Review
- Review
- Transposable Element Expression in Acute Myeloid Leukemia Transcriptome and Prognosis.Scientific reports · 2018Article
- Interaction with RXR is necessary for NPM-RAR-induced myeloid differentiation blockade.Leukemia research · 2013Article
- The recognition of N-glycans by the lectin ArtinM mediates cell death of a human myeloid leukemia cell line.PloS one · 2011Article
- Epigenetic remodeling of chromatin architecture: exploring tumor differentiation therapies in mesenchymal stem cells and sarcomas.Current stem cell research & therapy · 2010Review
- Retinoid signaling regulates breast cancer stem cell differentiation.Cell cycle (Georgetown, Tex.) · 2009Article
- Alpha-fetoprotein, stem cells and cancer: how study of the production of alpha-fetoprotein during chemical hepatocarcinogenesis led to reaffirmation of the stem cell theory of cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2008Review
- Mechanism of histone H1-stimulated glucocorticoid receptor DNA binding in vivo.Molecular and cellular biology · 2007Article
- Identification of a molecular signature for leukemic promyelocytes and their normal counterparts: Focus on DNA repair genes.Leukemia · 2006Article
- Pro-proliferative function of the long isoform of PML-RARalpha involved in acute promyelocytic leukemia.Oncogene · 2006Article
- The methyl-CpG binding protein MBD1 is required for PML-RARalpha function.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Article
- Alternative mRNA splicing of SMRT creates functional diversity by generating corepressor isoforms with different affinities for different nuclear receptors.The Journal of biological chemistry · 2005Article
- Leukemia: stem cells, maturation arrest, and differentiation therapy.Stem cell reviews · 2005Review
- PML-RARA-RXR oligomers mediate retinoid and rexinoid/cAMP cross-talk in acute promyelocytic leukemia cell differentiation.The Journal of experimental medicine · 2004Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PML-RAR is an oncogenic transcription factor forming in acute promyelocytic leukemias (APL) because of a chromosomal translocation. Without its ligand, retinoic acid (RA), PML-RAR functions as a constitutive transcriptional repressor, abnormally associating with the corepressor-histone deacetylase complex and blocking hematopoietic differentiation. In the presence of pharmacological concentrations of RA, PML-RAR activates transcription and stimulates differentiation. Even though it has been suggested that chromatin alteration is important for APL onset, the PML-RAR effect on chromatin of target promoters has not been investigated. Taking advantage of the Xenopus oocyte system, we compared the wild-type transcription factor RARalpha with PML-RAR as both transcriptional regulators and chromatin structure modifiers. Without RA, we found that PML-RAR is a more potent transcriptional repressor that does not require the cofactor RXR and produces a closed chromatin configuration. Surprisingly, repression by PML-RAR occurs through a further pathway that is independent of nucleosome deposition and histone deacetylation. In the presence of RA, PML-RAR is a less efficient transcriptional activator that is unable to modify the DNA nucleoprotein structure. We propose that PML-RAR, aside from its ability to recruit aberrant quantities of histone deacetylase complexes, has acquired additional repressive mechanisms and lost important activating functions; the comprehension of these mechanisms might reveal novel targets for antileukemic intervention.
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