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Status |
Public on Jan 31, 2013 |
Title |
RUNX1 is a key target gene in t(4;11) leukemias and contributes to gene activation by interacting with the AF4-MLL complex |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
|
Summary |
The Mixed Lineage Leukemia 1 protein (MLL1) is an important epigenetic regulator required for the maintenance of gene activation during development. MLL1 chromosome translocations produce novel fusion proteins that cause aggressive leukemias in humans. Individual MLL1 fusion proteins have distinct leukemic phenotypes even when expressed in the same cell type, but how this distinction is delineated on a molecular level is poorly understood. Here we highlight a unique molecular mechanism whereby MLL-AF4 specifically activates the RUNX1 gene and the RUNX1 protein interacts with the product of the reciprocal AF4-MLL translocation. These results support a mechanism of leukemic growth whereby two oncogenic fusion proteins cooperate by activating a target gene and then interacting directly with its downstream product
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Overall design |
ChIP-seq using RUNX1 antibody in SEM cells
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Contributor(s) |
Ballabio E, Geng H, Milne TA |
Citation(s) |
23352661 |
Submission date |
Nov 06, 2012 |
Last update date |
May 15, 2019 |
Contact name |
Erica Ballabio |
E-mail(s) |
erica.ballabio@imm.ox.ac.uk
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Phone |
0044 1865 222418
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Organization name |
Univeristy of Oxford
|
Department |
The Weatherall Institute of Molecular Medicine
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Lab |
Tom Milne
|
Street address |
headley way
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City |
Oxford |
ZIP/Postal code |
OX3 9DS |
Country |
United Kingdom |
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Platforms (1) |
GPL11154 |
Illumina HiSeq 2000 (Homo sapiens) |
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Samples (2) |
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Relations |
BioProject |
PRJNA179081 |
SRA |
SRP017083 |