Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Mol Cell Biol
2001 Jan 01;211:224-34. doi: 10.1128/MCB.21.1.224-234.2001.
Show Gene links
Show Anatomy links
Defining roles for HOX and MEIS1 genes in induction of acute myeloid leukemia.
Thorsteinsdottir U
,
Kroon E
,
Jerome L
,
Blasi F
,
Sauvageau G
.
???displayArticle.abstract???
Complex genetic and biochemical interactions between HOX proteins and members of the TALE (i.e., PBX and MEIS) family have been identified in embryonic development, and some of these interactions also appear to be important for leukemic transformation. We have previously shown that HOXA9 collaborates with MEIS1 in the induction of acute myeloid leukemia (AML). In this report, we demonstrate that HOXB3, which is highly divergent from HOXA9, also genetically interacts with MEIS1, but not with PBX1, in generating AML. In addition, we show that the HOXA9 and HOXB3 genes play key roles in establishing all the main characteristics of the leukemias, while MEIS1 functions only to accelerate the onset of the leukemic transformation. Contrasting the reported functional similarities between PREP1 and MEIS1, such as PBX nuclear retention, we also show that PREP1 overexpression is incapable of accelerating the HOXA9-induced AML, suggesting that MEIS1 function in transformation must entail more than PBX nuclear localization. Collectively, these data demonstrate that MEIS1 is a common leukemic collaborator with two structurally and functionally divergent HOX genes and that, in this collaboration, the HOX gene defines the identity of the leukemia.
Abu-Shaar,
Control of the nuclear localization of Extradenticle by competing nuclear import and export signals.
1999, Pubmed
Abu-Shaar,
Control of the nuclear localization of Extradenticle by competing nuclear import and export signals.
1999,
Pubmed
Azpiazu,
Functional and regulatory interactions between Hox and extradenticle genes.
1998,
Pubmed
Berthelsen,
Prep1, a novel functional partner of Pbx proteins.
1998,
Pubmed
Berthelsen,
The novel homeoprotein Prep1 modulates Pbx-Hox protein cooperativity.
1998,
Pubmed
Berthelsen,
The subcellular localization of PBX1 and EXD proteins depends on nuclear import and export signals and is modulated by association with PREP1 and HTH.
1999,
Pubmed
Borrow,
The t(7;11)(p15;p15) translocation in acute myeloid leukaemia fuses the genes for nucleoporin NUP98 and class I homeoprotein HOXA9.
1996,
Pubmed
Calvo,
Hoxa9 immortalizes a granulocyte-macrophage colony-stimulating factor-dependent promyelocyte capable of biphenotypic differentiation to neutrophils or macrophages, independent of enforced meis expression.
2000,
Pubmed
Chang,
Meis proteins are major in vivo DNA binding partners for wild-type but not chimeric Pbx proteins.
1997,
Pubmed
Ferretti,
The PBX-regulating protein PREP1 is present in different PBX-complexed forms in mouse.
1999,
Pubmed
Ferretti,
Segmental expression of Hoxb2 in r4 requires two separate sites that integrate cooperative interactions between Prep1, Pbx and Hox proteins.
2000,
Pubmed
Giampaolo,
Key functional role and lineage-specific expression of selected HOXB genes in purified hematopoietic progenitor differentiation.
1994,
Pubmed
Golub,
Molecular classification of cancer: class discovery and class prediction by gene expression monitoring.
1999,
Pubmed
Hawley,
Transforming function of the HOX11/TCL3 homeobox gene.
1997,
Pubmed
Jacobs,
Trimeric association of Hox and TALE homeodomain proteins mediates Hoxb2 hindbrain enhancer activity.
1999,
Pubmed
Jaw,
Direct interaction of two homeoproteins, homothorax and extradenticle, is essential for EXD nuclear localization and function.
2000,
Pubmed
Kamps,
A new homeobox gene contributes the DNA binding domain of the t(1;19) translocation protein in pre-B ALL.
1990,
Pubmed
Kroon,
Hoxa9 transforms primary bone marrow cells through specific collaboration with Meis1a but not Pbx1b.
1998,
Pubmed
Krosl,
Cellular proliferation and transformation induced by HOXB4 and HOXB3 proteins involves cooperation with PBX1.
1998,
Pubmed
,
Xenbase
Look,
Oncogenic transcription factors in the human acute leukemias.
1997,
Pubmed
Mann,
The specificity of homeotic gene function.
1995,
Pubmed
Monica,
Transformation properties of the E2a-Pbx1 chimeric oncoprotein: fusion with E2a is essential, but the Pbx1 homeodomain is dispensable.
1994,
Pubmed
Moskow,
Meis1, a PBX1-related homeobox gene involved in myeloid leukemia in BXH-2 mice.
1995,
Pubmed
Nakamura,
Cooperative activation of Hoxa and Pbx1-related genes in murine myeloid leukaemias.
1996,
Pubmed
Nakamura,
Fusion of the nucleoporin gene NUP98 to HOXA9 by the chromosome translocation t(7;11)(p15;p15) in human myeloid leukaemia.
1996,
Pubmed
Nakamura,
Identification of a new family of Pbx-related homeobox genes.
1996,
Pubmed
Nourse,
Chromosomal translocation t(1;19) results in synthesis of a homeobox fusion mRNA that codes for a potential chimeric transcription factor.
1990,
Pubmed
Pai,
The Homothorax homeoprotein activates the nuclear localization of another homeoprotein, extradenticle, and suppresses eye development in Drosophila.
1998,
Pubmed
Perkins,
Conditional immortalization of mouse myelomonocytic, megakaryocytic and mast cell progenitors by the Hox-2.4 homeobox gene.
1993,
Pubmed
Pöpperl,
Segmental expression of Hoxb-1 is controlled by a highly conserved autoregulatory loop dependent upon exd/pbx.
1995,
Pubmed
Rieckhof,
Nuclear translocation of extradenticle requires homothorax, which encodes an extradenticle-related homeodomain protein.
1997,
Pubmed
Ryoo,
Regulation of Hox target genes by a DNA bound Homothorax/Hox/Extradenticle complex.
1999,
Pubmed
Sauvageau,
Differential expression of homeobox genes in functionally distinct CD34+ subpopulations of human bone marrow cells.
1994,
Pubmed
Sauvageau,
Overexpression of HOXB3 in hematopoietic cells causes defective lymphoid development and progressive myeloproliferation.
1997,
Pubmed
,
Xenbase
Sauvageau,
Overexpression of HOXB4 in hematopoietic cells causes the selective expansion of more primitive populations in vitro and in vivo.
1995,
Pubmed
Schnabel,
HoxA9-mediated immortalization of myeloid progenitors requires functional interactions with TALE cofactors Pbx and Meis.
2000,
Pubmed
Shen,
AbdB-like Hox proteins stabilize DNA binding by the Meis1 homeodomain proteins.
1997,
Pubmed
Shen,
HOXA9 forms triple complexes with PBX2 and MEIS1 in myeloid cells.
1999,
Pubmed
Thorsteinsdottir,
Overexpression of HOXA10 in murine hematopoietic cells perturbs both myeloid and lymphoid differentiation and leads to acute myeloid leukemia.
1997,
Pubmed
Thorsteinsdottir,
Hox homeobox genes as regulators of normal and leukemic hematopoiesis.
1997,
Pubmed
Thorsteinsdottir,
The oncoprotein E2A-Pbx1a collaborates with Hoxa9 to acutely transform primary bone marrow cells.
1999,
Pubmed
