ArticleProceedings of the National Academy of Sciences of the United States of America1997
Cell death induction by the acute promyelocytic leukemia-specific PML/RARalpha fusion protein.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 66 citations in OpenAlex.
- PML-driven sumoylation of PML::RARA-bound repressors drives hematopoietic progenitor immortalization.The Journal of experimental medicine · 2026Article
- Low HOX gene expression in PML-RARα-positive leukemia results from suppressed histone demethylation.Epigenetics · 2018Article
- Article
- PML-RARA can increase hematopoietic self-renewal without causing a myeloproliferative disease in mice.The Journal of clinical investigation · 2011Article
- E3 ligase FLRF (Rnf41) regulates differentiation of hematopoietic progenitors by governing steady-state levels of cytokine and retinoic acid receptors.Experimental hematology · 2008Article
- Pro-proliferative function of the long isoform of PML-RARalpha involved in acute promyelocytic leukemia.Oncogene · 2006Article
- Direct evidence for cooperating genetic events in the leukemic transformation of normal human hematopoietic cells.Leukemia · 2005Article
- Neutrophil elastase is important for PML-retinoic acid receptor alpha activities in early myeloid cells.Molecular and cellular biology · 2005Article
- Concepts of human leukemic development.Oncogene · 2004Review
- Acute promyelocytic leukemia: where does it stem from?Leukemia · 2004Review
- Pondering the promyelocytic leukemia protein (PML) puzzle: possible functions for PML nuclear bodies.Molecular and cellular biology · 2002Review
- PML/RARalpha and FLT3-ITD induce an APL-like disease in a mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Review
- Common themes in the pathogenesis of acute myeloid leukemia.Oncogene · 2001Review
- BCL-2 cooperates with promyelocytic leukemia retinoic acid receptor alpha chimeric protein (PMLRARalpha) to block neutrophil differentiation and initiate acute leukemia.The Journal of experimental medicine · 2001Article
- Colocalization and heteromerization between the two human oncogene POZ/zinc finger proteins, LAZ3 (BCL6) and PLZF.Oncogene · 2000Article
- Article
- Article
- Overexpressed BCL6 (LAZ3) oncoprotein triggers apoptosis, delays S phase progression and associates with replication foci.Oncogene · 1999Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PML/RARalpha is the abnormal protein product generated by the acute promyelocytic leukemia-specific t(15;17). Expression of PML/RARalpha in hematopoietic precursor cell lines induces block of differentiation and promotes survival. We report here that PML/RARalpha has a potent growth inhibitory effect on all nonhematopoietic cell lines and on the majority of the hematopoietic cell lines tested. Inducible expression of PML/RARalpha in fibroblasts demonstrated that the basis for the growth suppression is induction of cell death. Deletion of relevant promyelocytic leukemia (PML) and retinoic acid receptor (RARalpha) domains within the fusion protein revealed that its growth inhibitory effect depends on the integrity of the PML aminoterminal region (RING, B1, B2, and coiled coil regions) and the RARalpha DNA binding region. Analysis of the nuclear localization of the same PML/RARalpha deletion mutants by immunofluorescence and cell fractionation revealed that the biological activity of the fusion protein correlates with its microspeckled localization and its association to the nuclear matrix. The PML aminoterminal region, but not the RARalpha zinc fingers, is required for the proper nuclear localization of PML/RARalpha. We propose that the matrix-associated microspeckles are the active sites of PML/RARalpha and that targeting of RARalpha sequences to this specific nuclear subdomain through PML sequences is crucial to the activity of the fusion protein on survival regulation.
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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.