ArticleMolecular and cellular biology2001
Arsenic trioxide is a potent inhibitor of the interaction of SMRT corepressor with Its transcription factor partners, including the PML-retinoic acid receptor alpha oncoprotein found in human acute promyelocytic leukemia.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 59 citations in OpenAlex.
- Distinct biochemical properties of the class I histone deacetylase complexes.Current opinion in chemical biology · 2022Review
- Differentiation therapy for myeloid malignancies: beyond cytotoxicity.Blood cancer journal · 2021Review
- Immune Classification and Immune Landscape Analysis of Triple-Negative Breast Cancer.Frontiers in genetics · 2021Article
- Arsenic trioxide inhibits liver cancer stem cells and metastasis by targeting SRF/MCM7 complex.Cell death & disease · 2019Article
- Nucleus accumbens associated 1 is recruited within the promyelocytic leukemia nuclear body through SUMO modification.Cancer science · 2015Article
- The impact of arsenic trioxide and all-trans retinoic acid on p53 R273H-codon mutant glioblastoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Arsenic trioxide stabilizes accumulations of adeno-associated virus virions at the perinuclear region, increasing transduction in vitro and in vivo.Journal of virology · 2013Article
- Nuclear receptor co-repressors are required for the histone-deacetylase activity of HDAC3 in vivo.Nature structural & molecular biology · 2013Article
- Thyroid hormone receptor β1 domains responsible for the antagonism with the ras oncogene: role of corepressors.Oncogene · 2011Article
- Aberrant corepressor interactions implicated in PML-RAR(alpha) and PLZF-RAR(alpha) leukemogenesis reflect an altered recruitment and release of specific NCoR and SMRT splice variants.The Journal of biological chemistry · 2011Article
- Regulation of SMRT corepressor dimerization and composition by MAP kinase phosphorylation.Molecular and cellular endocrinology · 2011Article
- Article
- Response of SMRT (silencing mediator of retinoic acid and thyroid hormone receptor) and N-CoR (nuclear receptor corepressor) corepressors to mitogen-activated protein kinase kinase kinase cascades is determined by alternative mRNA splicing.Molecular endocrinology (Baltimore, Md.) · 2007Article
- Nuclear IKK activity leads to dysregulated notch-dependent gene expression in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Review
- Arsenic trioxide affects signal transducer and activator of transcription proteins through alteration of protein tyrosine kinase phosphorylation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2006Article
- Arsenic trioxide inhibits nuclear receptor function via SEK1/JNK-mediated RXRalpha phosphorylation.The Journal of clinical investigation · 2005Article
- Retinoic acid and arsenic trioxide cooperate for apoptosis through phosphorylated RXR alpha.Oncogene · 2005Article
- Targeting fusion protein/corepressor contact restores differentiation response in leukemia cells.The EMBO journal · 2005Article
- SMRT and N-CoR corepressors are regulated by distinct kinase signaling pathways.The Journal of biological chemistry · 2004Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The SMRT corepressor complex participates in transcriptional repression by a diverse array of vertebrate transcription factors. The ability to recruit SMRT appears to play a crucial role in leukemogenesis by the PML-retinoic acid receptor alpha (RARalpha) oncoprotein, an aberrant nuclear hormone receptor implicated in human acute promyelocytic leukemia (APL). Arsenite induces clinical remission of APL through a incompletely understood mechanism. We report here that arsenite is a potent inhibitor of the interaction of SMRT with its transcription factor partners, including PML-RARalpha. Arsenite operates, in part, through a mitogen-activated protein (MAP) kinase cascade culminating in phosphorylation of the SMRT protein, dissociation of SMRT from its nuclear receptor partners, and a relocalization of SMRT out of the nucleus into the cytoplasm of the cell. Conversely, inhibition of this MAP kinase cascade attenuates the effects of arsenite on APL cells. Our results implicate SMRT as an important biological target for the actions of arsenite in both normal and neoplastic cells.
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