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Interaction of c-Myb with p300 is required for the induction of acute myeloid leukemia (AML) by human AML oncogenes

ChEBI2012-12-31 更新2026-07-21 收录

白血病分子机制

致癌蛋白相互作用

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-34224 数据链接链接失效反馈

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资源简介：

Interaction of c-Myb with p300 is required for the induction of acute myeloid leukemia (AML) by human AML oncogenes

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创建时间：

2012-12-31

白血病分子机制

CD40

In this experiment we in vitro activated CLL cells on a layer of fibroblasts expressing CD40L (3T40) or nothing (3T3) for 48 hours. After the 48 hours, cells were taken off the fibroblasts and sorted

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TET2 and DNMT3A Mutations Exert Divergent Effects on DNA Repair and Sensitivity of Leukemia Cells to PARP Inhibitors

白血病分子机制

PARP抑制剂敏感性

TET2 and DNMT3A regulate the sensitivity to PARP inhibitor To model the somatic loss-of-function mutations found in human blood diseases, mice with conditional inactivation of Dnmt3a and Tet2 in the h

NIAID Data Ecosystem40

Overexpression of the Catalytically Impaired Taspase1 T234V or Taspase1 D233A Variants Does Not Have a Dominant Negative Effect in T(4;11) Leukemia Cells

白血病分子机制

Taspase1酶活性

BackgroundThe chromosomal translocation t(4;11)(q21;q23) is associated with high-risk acute lymphoblastic leukemia of infants. The resulting AF4•MLL oncoprotein becomes activated by Taspase1 hydrolysi

NIAID Data Ecosystem30

Additional file 2 of NSD2 E1099K drives relapse in pediatric acute lymphoblastic leukemia by disrupting 3D chromatin organization

白血病分子机制

染色质结构

Additional file 2. stable_genomic_loci.bed LOLA Analysis File of stable ATAC-seq peaks.

NIAID Data Ecosystem50

METTL3 affects FLT3-ITD+ acute myeloid leukemia by mediating autophagy by regulating PSMA3-AS1 stability

白血病分子机制

自噬调控

The study was designed to explore the role of PSMA3-AS1 in initiation and progression of acute myeloid leukemia (AML) and investigate its action mechanism. Expression of PSMA3-AS1, miR-20a-5p and ATG1

NIAID Data Ecosystem30

Interaction of c-Myb with p300 is required for the induction of acute myeloid leukemia (AML) by human AML oncogenes

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