The leukemogenic AF4-MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures. (Q54637392)

1 June 2018

title

The leukemogenic AF4-MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures. (English)

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1 June 2018

author

Theodor Dingermann

10

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Rolf Marschalek

11

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author name string

A Benedikt

1

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S Baltruschat

2

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B Scholz

3

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A Bursen

4

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T N Arrey

5

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B Meyer

6

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L Varagnolo

7

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A M Müller

8

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M Karas

9

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publication date

29 October 2010

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published in

Leukemia

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volume

25

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page(s)

135-144

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issue

1

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https://scigraph.springernature.com/pub.10.1038/leu.2010.249

exact match

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cites work

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A murine Mll-AF4 knock-in model results in lymphoid and myeloid deregulation and hematologic malignancy

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H3K79 methylation profiles define murine and human MLL-AF4 leukemias

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Interaction of AF4 wild-type and AF4.MLL fusion protein with SIAH proteins: indication for t(4;11) pathobiology?

21 January 2018

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Taspase1: a threonine aspartase required for cleavage of MLL and proper HOX gene expression

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The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4.

21 January 2018

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MLL fusion partners AF4 and AF9 interact at subnuclear foci

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Misguided transcriptional elongation causes mixed lineage leukemia

21 January 2018

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A role for the MLL fusion partner ENL in transcriptional elongation and chromatin modification

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Methylation of H3-lysine 79 is mediated by a new family of HMTases without a SET domain

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DOT1L/KMT4 recruitment and H3K79 methylation are ubiquitously coupled with gene transcription in mammalian cells

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MCEF, the newest member of the AF4 family of transcription factors involved in leukemia, is a positive transcription elongation factor-b-associated protein

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The mixed-lineage leukemia fusion partner AF4 stimulates RNA polymerase II transcriptional elongation and mediates coordinated chromatin remodeling

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MLL targets SET domain methyltransferase activity to Hox gene promoters

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Chromatin flow cytometry identifies changes in epigenetic cell states

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The bromodomain protein Brd4 is a positive regulatory component of P-TEFb and stimulates RNA polymerase II-dependent transcription

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WDR5 associates with histone H3 methylated at K4 and is essential for H3 K4 methylation and vertebrate development

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Physical association and coordinate function of the H3 K4 methyltransferase MLL1 and the H4 K16 acetyltransferase MOF

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The C-terminal SET domains of ALL-1 and TRITHORAX interact with the INI1 and SNR1 proteins, components of the SWI/SNF complex

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Leukemic HRX fusion proteins inhibit GADD34-induced apoptosis and associate with the GADD34 and hSNF5/INI1 proteins

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Proteolysis of MLL family proteins is essential for taspase1-orchestrated cell cycle progression.

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E2F activation of S phase promoters via association with HCF-1 and the MLL family of histone H3K4 methyltransferases.

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Arginine methyltransferase CARM1 is a promoter-specific regulator of NF-kappaB-dependent gene expression

21 January 2018

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Recruitment of P-TEFb for stimulation of transcriptional elongation by the bromodomain protein Brd4

21 January 2018

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Brd4 coactivates transcriptional activation of NF-kappaB via specific binding to acetylated RelA

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Nucleophosmin/B23 regulates transcriptional activation of E2F1 via modulating the promoter binding of NF-kappaB, E2F1 and pRB.

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Nucleophosmin interacts with HEXIM1 and regulates RNA polymerase II transcription

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ALL-1 is a histone methyltransferase that assembles a supercomplex of proteins involved in transcriptional regulation

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Proteolytic cleavage of MLL generates a complex of N- and C-terminal fragments that confers protein stability and subnuclear localization

21 January 2018

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Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression

21 January 2018

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https://api.crossref.org/works/10.1038%2FLEU.2010.249

CARM1 but not its enzymatic activity is required for transcriptional coactivation of NF-kappaB-dependent gene expression

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.249

Combined effects of the two reciprocal t(4;11) fusion proteins MLL.AF4 and AF4.MLL confer resistance to apoptosis, cell cycling capacity and growth transformation.

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.249

AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.249

A higher-order complex containing AF4 and ENL family proteins with P-TEFb facilitates oncogenic and physiologic MLL-dependent transcription

21 January 2018

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https://api.crossref.org/works/10.1038%2FLEU.2010.249

A conditional model of MLL-AF4 B-cell tumourigenesis using invertor technology

21 January 2018

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https://api.crossref.org/works/10.1038%2FLEU.2010.249

Purification of P-TEFb, a transcription factor required for the transition into productive elongation.

21 January 2018

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.249

inferred from DOI database lookup

7 January 2021

based on heuristic

Raf-1 kinase targets GA-binding protein in transcriptional regulation of the human immunodeficiency virus type 1 promoter.

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.249

inferred from DOI database lookup

7 January 2021

based on heuristic

The eleven-nineteen-leukemia protein ENL connects nuclear MLL fusion partners with chromatin

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.249

inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1038/LEU.2010.249

1 reference

1 June 2018

PubMed ID

21030982

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1 June 2018