(Q42815627)

7 November 2017

title

AML1-Evi-1 specifically transforms hematopoietic stem cells through fusion of the entire Evi-1 sequence to AML1. (English)

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7 November 2017

M Takeshita

1

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7 November 2017

M Ichikawa

2

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7 November 2017

E Nitta

3

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7 November 2017

S Goyama

4

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7 November 2017

T Asai

5

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7 November 2017

S Ogawa

6

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7 November 2017

S Chiba

7

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7 November 2017

M Kurokawa

8

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7 November 2017

publication date

13 March 2008

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7 November 2017

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7 November 2017

volume

22

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7 November 2017

issue

6

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7 November 2017

page(s)

1241-1249

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Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias

7 November 2017

cites work

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

The t(8;21) fusion protein interferes with AML-1B-dependent transcriptional activation

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

Identification of AML-1 and the (8;21) translocation protein (AML-1/ETO) as sequence-specific DNA-binding proteins: the runt homology domain is required for DNA binding and protein-protein interactions

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

t(8;21) breakpoints on chromosome 21 in acute myeloid leukemia are clustered within a limited region of a single gene, AML1

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

Consistent intergenic splicing and production of multiple transcripts between AML1 at 21q22 and unrelated genes at 3q26 in (3;21)(q26;q22) translocations

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

The chimeric genes AML1/MDS1 and AML1/EAP inhibit AML1B activation at the CSF1R promoter, but only AML1/MDS1 has tumor-promoter properties.

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

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

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

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

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

AML1 deletion in adult mice causes splenomegaly and lymphomas.

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

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

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

The leukemia-associated transcription repressor AML1/MDS1/EVI1 requires CtBP to induce abnormal growth and differentiation of murine hematopoietic cells

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

Oligomerization of Evi-1 regulated by the PR domain contributes to recruitment of corepressor CtBP

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

The oncoprotein Evi-1 represses TGF-beta signalling by inhibiting Smad3

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

The evi-1 oncoprotein inhibits c-Jun N-terminal kinase and prevents stress-induced cell death

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

Interaction of EVI1 with cAMP-responsive element-binding protein-binding protein (CBP) and p300/CBP-associated factor (P/CAF) results in reversible acetylation of EVI1 and in co-localization in nuclear speckles

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

Evi-1 transforming and repressor activities are mediated by CtBP co-repressor proteins

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

The corepressor CtBP interacts with Evi-1 to repress transforming growth factor beta signaling

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP.

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors.

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

The distal zinc finger domain of AML1/MDS1/EVI1 is an oligomerization domain involved in induction of hematopoietic differentiation defects in primary cells in vitro

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

MOZ-TIF2-induced acute myeloid leukemia requires the MOZ nucleosome binding motif and TIF2-mediated recruitment of CBP.

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2008.53

7 January 2021

Identifiers

DOI

10.1038/LEU.2008.53

1 reference

Dimensions Publication ID

7 November 2017

1052469845

0 references

1 reference