ArticleProceedings of the National Academy of Sciences of the United States of America2010
PML/RARalpha fusion protein transactivates the tissue factor promoter through a GAGC-containing element without direct DNA association.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- A machine learning model identifies M3-like subtype in AML based on PML/RARα targets.iScience · 2024Article
- Thrombosis in Myeloid Malignancies: From CHIP to AML.Cardiovascular & hematological disorders drug targets · 2024Review
- Review
- A PML/RARα direct target atlas redefines transcriptional deregulation in acute promyelocytic leukemia.Blood · 2021Article
- Absolute Circulating Leukemic Cells as a Risk Factor for Early Bleeding Events in Patients with Non-High-Risk Acute Promyelocytic Leukemia.Cancer management and research · 2021Article
- Observational
- Annexin A2-S100A10 heterotetramer is upregulated by PML/RARα fusion protein and promotes plasminogen-dependent fibrinolysis and matrix invasion in acute promyelocytic leukemia.Frontiers of medicine · 2017Article
- The DNA binding property of PML/RARA but not the integrity of PML nuclear bodies is indispensable for leukemic transformation.PloS one · 2014Article
- Phosphatidylserine index as a marker of the procoagulant phenotype of acute myelogenous leukemia cells.Physical biology · 2013Article
- Characterization of the thrombin generation potential of leukemic and solid tumor cells by calibrated automated thrombography.Haematologica · 2012Article
- Opposite regulation by PI3K/Akt and MAPK/ERK pathways of tissue factor expression, cell-associated procoagulant activity and invasiveness in MDA-MB-231 cells.Journal of hematology & oncology · 2012Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A severe coagulopathy is a life-threatening complication of acute promyelocytic leukemia (APL) and is ascribable mainly to the excessive levels of tissue factor (TF) in APL cells regulated in response to the promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) fusion protein. The underlying molecular mechanisms for this regulation remain ill-defined. With U937-PR9 cell lines stably expressing luciferase reporter gene under the control of different mutants of the TF promoter, both luciferase and ChIP data allowed the localization of the PML/RARalpha-responsive sequence in a previously undefined region of the TF promoter at position -230 to -242 devoid of known mammalian transcription factor binding sites. Within this sequence a GAGC motif (-235 to -238) was shown to be crucial because deletion or mutation of these nucleotides impaired both PML/RARalpha interaction and promoter transactivation. However, EMSA results showed that PML/RARalpha did not bind to DNA probes encompassing the -230 to -242 sequences, precluding a direct DNA association. Mutational experiments further suggest that the activator protein 1 (AP-1) sites of the TF promoter are dispensable for PML/RARalpha regulation. This study shows that PML/RARalpha transactivates the TF promoter through an indirect interaction with an element composed of a GAGC motif and the flanking nucleotides, independent of AP-1 binding.
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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.