MLL is essential for NUP98-HOXA9-induced leukemia

No abstract is available for this paper.

• Publication year

  2015

• Venue

  Leukemia

• Publication date

  2015-12-03

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/leu.2017.62PMID 28210005
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Essential role of PU.1 in maintenance of mixed lineage leukemia-associated leukemic stem cells

  2015cited by this paper
• Nucleoporin Nup98 associates with Trx/MLL and NSL histone-modifying complexes and regulates Hox gene expression.

  2014influential reference
• PML-RARα and its phosphorylation regulate pml oligomerization and HIPK2 stability.

  2013cited by this paper
• Requirement for Dot1l in murine postnatal hematopoiesis and leukemogenesis by MLL translocation.

  2011cited by this paper
• MLL-rearranged leukemia is dependent on aberrant H3K79 methylation by DOT1L.

  2011cited by this paper
• DOT1L, the H3K79 methyltransferase, is required for MLL-AF9-mediated leukemogenesis.

  2011cited by this paper
• CBX8, a polycomb group protein, is essential for MLL-AF9-induced leukemogenesis.

  2011cited by this paper
• NUP98 gene fusions and hematopoietic malignancies: common themes and new biologic insights.

  2011cited by this paper
• Amino-terminal Enhancer of Split (AES) Interacts with the Oncoprotein NUP98-HOXA9 and Enhances Its Transforming Ability*

  2011cited by this paper
• The nuclear pore complex: bridging nuclear transport and gene regulation

  2010cited by this paper
• MLL-AF9-induced leukemogenesis requires coexpression of the wild-type Mll allele.

  2010influential reference
• Inhibition of CRM1-mediated Nuclear Export of Transcription Factors by Leukemogenic NUP98 Fusion Proteins*

  2010cited by this paper
• Leukemogenic transformation by HOXA cluster genes.

  2010influential reference
• Inhibition of CRM1-Mediated Nuclear Export of Transcription FACTORS by Leukemogenic NUP98 Fusion Proteins.

  2009cited by this paper
• Malignant transformation initiated by Mll-AF9: gene dosage and critical target cells.

  2008cited by this paper
• NUP98–NSD1 links H3K36 methylation to Hox-A gene activation and leukaemogenesis

  2007cited by this paper
• Leukaemic transformation by CALM–AF10 involves upregulation of Hoxa5 by hDOT1L

  2006cited by this paper
• NUP98-HOXA9 induces long-term proliferation and blocks differentiation of primary human CD34+ hematopoietic cells.

  2006influential reference
• Identification and characterization of leukemia stem cells in murine MLL-AF9 acute myeloid leukemia.

  2006cited by this paper
• The Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions in acute myeloid leukemia.

  2006cited by this paper
• Transformation from committed progenitor to leukaemia stem cell initiated by MLL–AF9

  2006cited by this paper
• hDOT1L links histone methylation to leukemogenesis.

  2005cited by this paper
• Taspase1: a threonine aspartase required for cleavage of MLL and proper HOX gene expression.

  2003cited by this paper
• Structure of HoxA9 and Pbx1 bound to DNA: Hox hexapeptide and DNA recognition anterior to posterior.

  2003cited by this paper
• Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitors.

  2003cited by this paper
• MLL targets SET domain methyltransferase activity to Hox gene promoters.

  2002cited by this paper
• Leukemia proto-oncoprotein MLL is proteolytically processed into 2 fragments with opposite transcriptional properties.

  2002cited by this paper
• ALL-1 is a histone methyltransferase that assembles a supercomplex of proteins involved in transcriptional regulation.

  2002cited by this paper
• Nup98-HoxA9 immortalizes myeloid progenitors, enforces expression of Hoxa9, Hoxa7 and Meis1, and alters cytokine-specific responses in a manner similar to that induced by retroviral co-expression of Hoxa9 and Meis1

  2002cited by this paper
• NUP98–HOXA9 expression in hemopoietic stem cells induces chronic and acute myeloid leukemias in mice

  2001cited by this paper
• CREB Binding Protein Interacts with Nucleoporin-Specific FG Repeats That Activate Transcription and Mediate NUP98-HOXA9 Oncogenicity

  1999influential reference
• Growth disturbance in fetal liver hematopoiesis of Mll-mutant mice.

  1998cited by this paper
• Hoxa9 transforms primary bone marrow cells through specific collaboration with Meis1a but not Pbx1b

  1998cited by this paper
• MLL, a mammalian trithorax-group gene, functions as a transcriptional maintenance factor in morphogenesis.

  1998cited by this paper
• The inv(11)(p15q22) chromosome translocation of de novo and therapy-related myeloid malignancies results in fusion of the nucleoporin gene, NUP98, with the putative RNA helicase gene, DDX10.

  1997influential reference
• Fusion of the nucleoporin gene NUP98 to HOXA9 by the chromosome translocation t(7;11)(p15;p15) in human myeloid leukaemia

  1996influential reference
• Altered Hox expression and segmental identity in Mll-mutant mice

  1995influential reference

• Phase-separating fusion proteins drive cancer by upsetting transcription regulation

  2025cites this paper
• Loss of NOL10 leads to impaired disease progression of NUP98::DDX10 leukemia

  2025influential citation
• NUP98 oncofusions in myeloid malignancies: An update on molecular mechanisms and therapeutic opportunities

  2024cites this paper
• Advances in the understanding of nuclear pore complexes in human diseases

  2024cites this paper
• Allogeneic stem cell transplantation can prolong the survival of patients with NUP98-rearranged acute myeloid leukemia

  2023cites this paper
• Phase-separated nuclear bodies of nucleoporin fusions promote condensation of MLL1/CRM1 and rearrangement of 3D genome structure.

  2023cites this paper
• HOXA9 transcription factor is a double-edged sword: from development to cancer progression

  2023cites this paper
• Therapeutic targeting in pediatric acute myeloid leukemia with aberrant HOX/MEIS1 expression

  2023cites this paper
• Phase-separating fusion proteins drive cancer by dysregulating transcription through ectopic condensates

  2023cites this paper
• Emerging Targeted Therapy for Specific Genomic Abnormalities in Acute Myeloid Leukemia

  2022cites this paper
• HOXA9 has the hallmarks of a biological switch with implications in blood cancers

  2022cites this paper
• Phase-separated nuclear bodies of nucleoporin fusions, SET-NUP214 and NUP98-HOXA9, promote condensation of MLL1 and CRM1 to activate target genes

  2022influential citation
• SMARCA5 interacts with NUP98-NSD1 oncofusion protein and sustains hematopoietic cells transformation

  2022cites this paper
• HOXA9 acts as a regulatory switch in acute myeloid leukaemia and myeloproliferative neoplasms

  2021cites this paper
• HBO1-MLL interaction promotes AF4/ENL/P-TEFb-mediated leukemogenesis

  2021cites this paper
• HOXD13 promotes the malignant progression of colon cancer by upregulating PTPRN2

  2021cites this paper
• A genetic screen in Drosophila uncovers the multifaceted properties of the NUP98-HOXA9 oncogene

  2021cites this paper
• The Retinoblastoma Tumor Suppressor Is Required for the NUP98-HOXA9-Induced Aberrant Nuclear Envelope Phenotype

  2021cites this paper
• Phase Separation Mediates NUP98 Fusion Oncoprotein Leukemic Transformation

  2021cites this paper
• Mechanistic insights and potential therapeutic targets for NUP98-rearranged hematologic malignancies.

  2020cites this paper
• Epigenetic Regulators as the Gatekeepers of Hematopoiesis.

  2020cites this paper
• DNA Methylation Clusters and Their Relation to Cytogenetic Features in Pediatric AML

  2020cites this paper
• Alpha lipoic acid promotes development of hematopoietic progenitors derived from human embryonic stem cells by antagonizing ROS signals

  2020cites this paper
• Nuclear Periphery Takes Center Stage: The Role of Nuclear Pore Complexes in Cell Identity and Aging.

  2020cites this paper
• Disclosing the Interactome of Leukemogenic NUP98-HOXA9 and SET-NUP214 Fusion Proteins Using a Proteomic Approach

  2020cites this paper
• CDK6 is an essential direct target of NUP98-fusion proteins in acute myeloid leukemia.

  2020cites this paper
• The molecular functions of common and atypical MLL fusion protein complexes.

  2020cites this paper
• Nucleoporin 153 links nuclear pore complex to chromatin architecture by mediating CTCF and cohesin binding

  2020cites this paper
• The Nuclear Pore Complex in Cell Type-Specific Chromatin Structure and Gene Regulation.

  2019cites this paper
• The Hematopoietic Oxidase NOX2 Regulates Self-Renewal of Leukemic Stem Cells

  2019cites this paper
• Chromatin-bound CRM1 recruits SET-Nup214 and NPM1c onto HOX clusters causing aberrant HOX expression in leukemia cells

  2019cites this paper
• NUP214 in Leukemia: It’s More than Transport

  2019cites this paper
• The Role of the HOXA Gene Family in Acute Myeloid Leukemia

  2019cites this paper
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  2019cites this paper
• Risks of second primary malignancies among Chinese cancer survivors at a single center during 2002–2016

  2018cites this paper
• Nuclear Pore Complexes in the Organization and Regulation of the Mammalian Genome

  2018cites this paper
• Role of HOX Genes in Stem Cell Differentiation and Cancer

  2018cites this paper
• Jefferson Digital

  year unknowncites this paper
• NOL10 is required for NUP98-DDX10 leukemia

  year unknowncites this paper