(Q57615428)

1

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Pu Zhang

2

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Hideyo Hirai

3

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Shannon Elf

4

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Xiaomei Yan

5

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Zhao Chen

6

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Steffen Koschmieder

7

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Yutaka Okuno

8

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Tajhal Dayaram

9

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Joseph D Growney

10

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Ramesh A Shivdasani

11

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D Gary Gilliland

12

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Nancy A Speck

13

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Stephen D Nimer

https://scigraph.springernature.com/pub.10.1038/ng.2007.7

14

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language of work or name

English

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publication date

11 November 2007

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published in

Nature Genetics

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volume

40

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issue

1

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page(s)

51-60

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exact match

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cites work

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Combinatorial signaling in the specification of unique cell fates

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Disruption of differentiation in human cancer: AML shows the way.

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Role of transcription factors C/EBPalpha and PU.1 in normal hematopoiesis and leukemia.

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Hematopoietic cytokines, transcription factors and lineage commitment

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Point mutations in the RUNX1/AML1 gene: another actor in RUNX leukemia

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High incidence of somatic mutations in the AML1/RUNX1 gene in myelodysplastic syndrome and low blast percentage myeloid leukemia with myelodysplasia

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AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis

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Disruption of the Cbfa2 gene causes necrosis and hemorrhaging in the central nervous system and blocks definitive hematopoiesis

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Role of RUNX1 in adult hematopoiesis: analysis of RUNX1-IRES-GFP knock-in mice reveals differential lineage expression

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Runx1 is expressed in adult mouse hematopoietic stem cells and differentiating myeloid and lymphoid cells, but not in maturing erythroid cells

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AML-1 is required for megakaryocytic maturation and lymphocytic differentiation, but not for maintenance of hematopoietic stem cells in adult hematopoiesis

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Loss of Runx1 perturbs adult hematopoiesis and is associated with a myeloproliferative phenotype.

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AML1 deletion in adult mice causes splenomegaly and lymphomas.

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The 8;21 translocation in leukemogenesis

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Core-binding factors in hematopoiesis and immune function

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Uncovering regulatory pathways that affect hematopoietic stem cell function using 'genetical genomics'.

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Runt and Lozenge function in Drosophila development

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Lymphoid cell growth and transformation are suppressed by a key regulatory element of the gene encoding PU.1.

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Dynamic regulation of PU.1 expression in multipotent hematopoietic progenitors

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Mutations of the PU.1 Ets domain are specifically associated with murine radiation-induced, but not human therapy-related, acute myeloid leukaemia

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Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.

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Cooperating cancer-gene identification through oncogenic-retrovirus-induced insertional mutagenesis

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PU.1 is a suppressor of myeloid leukemia, inactivated in mice by gene deletion and mutation of its DNA binding domain.

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Regulation of the PU.1 gene by distal elements

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Expression of a conditional AML1-ETO oncogene bypasses embryonic lethality and establishes a murine model of human t(8;21) acute myeloid leukemia

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Regulation of B lymphocyte and macrophage development by graded expression of PU.1.

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CCAAT enhancer-binding protein (C/EBP) and AML1 (CBF alpha2) synergistically activate the macrophage colony-stimulating factor receptor promoter

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A clonogenic common myeloid progenitor that gives rise to all myeloid lineages

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Myeloid or lymphoid promiscuity as a critical step in hematopoietic lineage commitment.

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Spi-1/PU.1 transgenic mice develop multistep erythroleukemias

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The myeloid master regulator transcription factor PU.1 is inactivated by AML1-ETO in t(8;21) myeloid leukemia

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