ArticleThe EMBO journal1992
Structure, localization and transcriptional properties of two classes of retinoic acid receptor alpha fusion proteins in acute promyelocytic leukemia (APL): structural similarities with a new family of oncoproteins.
Article in The EMBO journal, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
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Who cites it
133 citing papers in PubMed, 429 citations in OpenAlex.
- History of Developing Acute Promyelocytic Leukemia Treatment and Role of Promyelocytic Leukemia Bodies.Cancers · 2024Review
- Conformational exchange at a CStructure (London, England : 1993) · 2023Article
- The interactions between PML nuclear bodies and small and medium size DNA viruses.Virology journal · 2023Review
- Alterations induced by the PML-RARα oncogene revealed by image cross correlation spectroscopy.Biophysical journal · 2022Article
- A PML/RARα direct target atlas redefines transcriptional deregulation in acute promyelocytic leukemia.Blood · 2021Article
- Article
- [Involvement of PML proteins in treatment of acute promyelocytic leukemia with arsenic trioxide].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Review
- Pml nuclear body disruption cooperates in APL pathogenesis and impairs DNA damage repair pathways in mice.Blood · 2018Article
- Deficiency of SUMO-specific protease 1 induces arsenic trioxide-mediated apoptosis by regulating XBP1 activity in human acute promyelocytic leukemia.Oncology letters · 2016Article
- PML isoforms IV and V contribute to adenovirus-mediated oncogenic transformation by functionally inhibiting the tumor-suppressor p53.Oncogene · 2016Article
- Sp100 isoform-specific regulation of human adenovirus 5 gene expression.Journal of virology · 2014Article
- Oxidative stress-induced assembly of PML nuclear bodies controls sumoylation of partner proteins.The Journal of cell biology · 2014Article
- Differential Roles of PML Isoforms.Frontiers in oncology · 2013Article
- The adenoviral oncogene E1A-13S interacts with a specific isoform of the tumor suppressor PML to enhance viral transcription.Journal of virology · 2013Article
- Emerging Cellular Functions of Cytoplasmic PML.Frontiers in oncology · 2013Article
- PML regulates PER2 nuclear localization and circadian function.The EMBO journal · 2012Article
- SUMO pathway dependent recruitment of cellular repressors to herpes simplex virus type 1 genomes.PLoS pathogens · 2011Article
- Entrapment of viral capsids in nuclear PML cages is an intrinsic antiviral host defense against varicella-zoster virus.PLoS pathogens · 2011Article
- Article
- SUMO modification of E1B-55K oncoprotein regulates isoform-specific binding to the tumour suppressor protein PML.Oncogene · 2010Article
73 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute promyelocytic leukemia (APL) is due to a chromosomal t(15;17) translocation which involves a novel human gene, Myl, (also named PML) and the retinoic acid (RA) receptor alpha (RAR-alpha) gene. We report here the characterization of Myl and of the reciprocal MylRAR (PMLRAR) and RARMyl (RARPML) fusion transcripts which are found in two classes of APL patients. Myl displays similarities with a new family of proteins of which some members are fused to protooncogenes in the transforming proteins RFP-ret and T18. The speckled nuclear localization of Myl, as well as its sequence homology with the 52 kDa component of the RO/SSA ribonucleoprotein particle, suggest that Myl may be present in a ribonucleoprotein complex. In contrast to both Myl and RAR-alpha whose localization is essentially nuclear in the presence or absence of RA, MylRAR which is largely cytoplasmic in the absence of RA appears to be translocated to the nucleus in the presence of RA. Myl and MylRAR can associate in vitro and this association is mediated by a coiled coil in the Myl sequence. In vivo this association results in a colocalization of Myl and MylRAR which is identical to that of MylRAR alone. Studies of activation of transcription from the promoters of several RA target genes indicate that MylRARs have altered transcription activation properties when compared with RAR-alpha. Most notably, MylRAR represses markedly the activity of some RA target promoters in the absence of RA. Western blot analyses of patient samples show that MylRAR is expressed to a much higher level than wild type RAR-alpha originating from the normal allele. Taken together, these results suggest that MylRAR may interfere in a dominant manner with both Myl and RAR functions.
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