ArticleThe Journal of biological chemistry2010
ASXL1 represses retinoic acid receptor-mediated transcription through associating with HP1 and LSD1.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 39 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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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
39 citing papers in PubMed, 88 citations in OpenAlex.
- LINC00586 Represses ASXL1 Expression Thus Inducing Epithelial-To-Mesenchymal Transition of Colorectal Cancer Cells Through LSD1-Mediated H3K4me2 Demethylation.Frontiers in pharmacology · 2022Article
- BAP1 complex promotes transcription by opposing PRC1-mediated H2A ubiquitylation.Nature communications · 2019Article
- Familial hematological malignancies: ASXL1 gene investigation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016Article
- Epigenetic regulators and their impact on therapy in acute myeloid leukemia.Haematologica · 2016Review
- The BAP1/ASXL2 Histone H2A Deubiquitinase Complex Regulates Cell Proliferation and Is Disrupted in Cancer.The Journal of biological chemistry · 2015Article
- Knockdown of SALL4 Protein Enhances All-trans Retinoic Acid-induced Cellular Differentiation in Acute Myeloid Leukemia Cells.The Journal of biological chemistry · 2015Article
- Article
- BAALC expression: a suitable marker for prognostic risk stratification and detection of residual disease in cytogenetically normal acute myeloid leukemia.Blood cancer journal · 2014Article
- Functional and cancer genomics of ASXL family members.British journal of cancer · 2013Review
- Unliganded progesterone receptor-mediated targeting of an RNA-containing repressive complex silences a subset of hormone-inducible genes.Genes & development · 2013Article
- Mutations in epigenetic modifiers in the pathogenesis and therapy of acute myeloid leukemia.Blood · 2013Review
- Review
- The JAK2 gene as a protagonist in chronic myeloproliferative neoplasms.Revista brasileira de hematologia e hemoterapia · 2013Article
- Additional sex combs-like 2 is required for polycomb repressive complex 2 binding at select targets.PloS one · 2013Article
- ASXL1 exon 12 mutations are frequent in AML with intermediate risk karyotype and are independently associated with an adverse outcome.Leukemia · 2013Article
- The genetic basis of phenotypic heterogeneity in myelodysplastic syndromes.Nature reviews. Cancer · 2012Review
- Role of TET2 and ASXL1 mutations in the pathogenesis of myeloproliferative neoplasms.Hematology/oncology clinics of North America · 2012Review
- ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression.Cancer cell · 2012Article
- Mutations in ASXL1 are associated with poor prognosis across the spectrum of malignant myeloid diseases.Journal of hematology & oncology · 2012Review
- Chronic myelomonocytic leukemia and atypical chronic myeloid leukemia: novel pathogenetic lesions.Seminars in oncology · 2012Review
Corrections and comments
- Retraction · 2015-03-06Notice - Limited or No Information · Removed ·
- Retracted
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously suggested that ASXL1 (additional sex comb-like 1) functions as either a coactivator or corepressor for the retinoid receptors retinoic acid receptor (RAR) and retinoid X receptor in a cell type-specific manner. Here, we provide clues toward the mechanism underlying ASXL1-mediated repression. Transfection assays in HEK293 or H1299 cells indicated that ASXL1 alone possessing autonomous transcriptional repression activity significantly represses RAR- or retinoid X receptor-dependent transcriptional activation, and the N-terminal portion of ASXL1 is responsible for the repression. Amino acid sequence analysis identified a consensus HP1 (heterochromatin protein 1)-binding site (HP1 box, PXVXL) in that region. Systematic in vitro and in vivo assays revealed that the HP1 box in ASXL1 is critical for the interaction with the chromoshadow domain of HP1. Transcription assays with HP1 box deletion or HP1alpha knockdown indicated that HP1alpha is required for ASXL1-mediated repression. Furthermore, we found a direct interaction of ASXL1 with histone H3 demethylase LSD1 through the N-terminal region nearby the HP1-binding site. ASXL1 binding to LSD1 was greatly increased by HP1alpha, resulting in the formation of a ternary complex. LSD1 cooperates with ASXL1 in transcriptional repression, presumably by removing H3K4 methylation, an active histone mark, but not H3K9 methylation, a repressive histone mark recognized by HP1. This possibility was supported by chromatin immunoprecipitation assays followed by ASXL1 overexpression or knockdown. Overall, this study provides the first evidence that ASXL1 cooperates with HP1 to modulate LSD1 activity, leading to a change in histone H3 methylation and thereby RAR repression.
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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.