The t(8;21) fusion protein, AML1/ETO, transforms NIH3T3 cells and activates AP-1. (Q42816817)

7 November 2017

The t(8;21) fusion protein, AML1/ETO, transforms NIH3T3 cells and activates AP-1. (English)

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7 November 2017

Frank RC

1

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7 November 2017

Sun X

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7 November 2017

Berguido FJ

3

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7 November 2017

Jakubowiak A

4

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7 November 2017

Nimer SD

5

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7 November 2017

language of work or name

English

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publication date

1 March 1999

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7 November 2017

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7 November 2017

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7 November 2017

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7 November 2017

1701-1710

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1202459

7 November 2017

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The AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1

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The AML1/ETO fusion protein activates transcription of BCL-2

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AML1, AML2, and AML3, the human members of the runt domain gene-family: cDNA structure, expression, and chromosomal localization

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The MYND motif is required for repression of basal transcription from the multidrug resistance 1 promoter by the t(8;21) fusion protein

21 January 2018

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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

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

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

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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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What's up and down with histone deacetylation and transcription?

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Production of high-titer helper-free retroviruses by transient transfection

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The Bcr-Abl leukemia oncogene activates Jun kinase and requires Jun for transformation

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The human leukemia oncogene bcr-abl abrogates the anchorage requirement but not the growth factor requirement for proliferation

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21 January 2018

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21 January 2018

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The t(8;21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation

21 January 2018

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The PML-retinoic acid receptor alpha translocation converts the receptor from an inhibitor to a retinoic acid-dependent activator of transcription factor AP-1

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7 January 2021

Indirect and direct disruption of transcriptional regulation in cancer: E2F and AML-1.

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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

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7 January 2021

An acute myeloid leukemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms.

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7 January 2021

Identifiers

DOI

10.1038/SJ.ONC.1202459

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Dimensions Publication ID

7 November 2017

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