+ |
AML1-ETO | down-regulates activity
binding
|
CEBPA |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255672 |
|
|
Homo sapiens |
Leukemia Cell |
pmid |
sentence |
11283671 |
Here we show that AML1–ETO blocks C/EBPα –dependent activation of its own promoter and thereby inhibits autoregulation. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255700 |
|
|
Homo sapiens |
U-937 Cell |
pmid |
sentence |
11283671 |
AML1–ETO inhibits CEBPA autoregulation in myeloid cells.[…]It was also demonstrated that AML1–ETO and C/EBPα physically interact in vivo. |
|
Publications: |
2 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, Onco-fusion proteins in AML |
+ |
AML1-ETO | down-regulates quantity by repression
transcriptional regulation
|
PTPRC |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255686 |
|
|
Mus musculus |
Leukemia Cell |
pmid |
sentence |
22740448 |
Chromosome translocation 8q22;21q22 [t(8;21)] is commonly associated with acute myeloid leukemia (AML), and the resulting AML1-ETO fusion proteins are involved in the pathogenesis of AML. To identify novel molecular and therapeutic targets, we performed combined gene expression microarray and promoter occupancy (ChIP-chip) profiling using Lin(-)/Sca1(-)/cKit(+) cells, the major leukemia cell population, from an AML mouse model induced by AML1-ETO9a (AE9a).CD45, a protein tyrosine phosphatase and a negative regulator of cytokine/growth factor receptor and JAK/STAT signaling, is among those targets. Its expression is substantially down-regulated in leukemia cells. Consequently, JAK/STAT signaling is enhanced. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
+ |
AML1-ETO | up-regulates quantity by expression
transcriptional regulation
|
PTGS2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255683 |
|
|
Mus musculus |
Bone Marrow Cell |
pmid |
sentence |
23645839 |
AML1-ETO (AE) is an oncogene that plays an important role in inducing self-renewal of hematopoietic stem/progenitor cells (HSPCs), leading to the development of leukemia stem cells. Here, we show that AE also induces expression of the Cox-2 gene and activates β-catenin in mouse bone marrow cells. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
+ |
AML1-ETO | down-regulates activity
binding
|
JUN |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255670 |
|
|
Homo sapiens |
Kasumi-1 Cell |
pmid |
sentence |
12393465 |
Here we show that AML1-ETO blocks the transcriptional activity of PU.1 by displacing its coactivator c-Jun. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
+ |
AML1-ETO | up-regulates quantity by expression
transcriptional regulation
|
KIT |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255699 |
|
|
Homo sapiens |
|
pmid |
sentence |
29236325 |
We report here that AML1/ETO transactivates c-KIT expression through directly binding to and mediating the long-range interaction between the promoter and intronic enhancer regions of c-KIT. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML |
+ |
AML1-ETO | down-regulates activity
binding
|
Core Binding Factor complex |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256100 |
|
|
Homo sapiens |
|
pmid |
sentence |
15829516 |
Two classes of models can describe how AML1-ETO could interfere with normal AML1 activity. First, because AML1-ETO has the potential to interact with AML1 co-factors (such as CBFβ) through its RD, it could act as a dominant-negative molecule by competing with AML1 for these co-factors. Although AML1-ETO has been shown to interact with CBFβ and repress the expression of AML1-regulated genes in vitro and in cell culture, the available data do not distinguish between these two models. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | AML1-ETO in AML |
+ |
AML1-ETO | up-regulates activity
binding
|
AP1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260094 |
|
|
Homo sapiens |
Kasumi-1 Cell |
pmid |
sentence |
10208431 |
The AML1/ETO fusion protein is essential to the development of t(8;21) acute myeloid leukemia (AML) and is well recognized for its dominant-negative effect on the coexisting wild-type protein AML1. On physical interaction, AML1/ETO can form a complex with wild-type AML1 on chromatin, and the runt homology domain of both proteins are responsible for their interactions. More importantly, the relative binding signals of AML1 and AML1/ETO on chromatin determine which genes are repressed or activated by AML1/ETO. Further analysis of coregulators indicates that AML1/ETO transactivates gene expression through recruiting AP-1 to the AML1/ETO-AML1 complex. AML1/ETO transactivates gene expression through recruiting AP-1 to the AML1/ETO-AML1 complex |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, Onco-fusion proteins in AML |
+ |
AML1-ETO | down-regulates quantity by repression
transcriptional regulation
|
JAK2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260120 |
|
|
Mus musculus |
Leukemia Cell |
pmid |
sentence |
22740448 |
Chromosome translocation 8q22;21q22 [t(8;21)] is commonly associated with acute myeloid leukemia (AML), and the resulting AML1-ETO fusion proteins are involved in the pathogenesis of AML. To identify novel molecular and therapeutic targets, we performed combined gene expression microarray and promoter occupancy (ChIP-chip) profiling using Lin(-)/Sca1(-)/cKit(+) cells, the major leukemia cell population, from an AML mouse model induced by AML1-ETO9a (AE9a).CD45, a protein tyrosine phosphatase and a negative regulator of cytokine/growth factor receptor and JAK/STAT signaling, is among those targets. Its expression is substantially down-regulated in leukemia cells. Consequently, JAK/STAT signaling is enhanced. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, Onco-fusion proteins in AML |
+ |
AML1-ETO | down-regulates quantity by repression
transcriptional regulation
|
hsa-mir-223 |
0.4 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255797 |
|
|
Mus musculus |
|
pmid |
sentence |
25477897 |
The three miR-29 family members in mouse bone marrow cells reduced the level of TET2 as well as its metabolic by-product, 5hmC |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | Acute Myeloid Leukemia |
+ |
AML1-ETO | down-regulates
transcriptional regulation
|
CDKN2A |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255677 |
|
|
Homo sapiens |
|
pmid |
sentence |
12091906 |
We have identified the p14(ARF) tumor suppressor, a mediator of the p53 oncogene checkpoint, as a direct transcriptional target of AML1 ETO. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, Onco-fusion proteins in AML |
+ |
AML1-ETO | down-regulates activity
binding
|
SPI1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255671 |
|
|
Homo sapiens |
CV-1 Cell |
pmid |
sentence |
18519037 |
We found that AML1-ETO is able to inhibit Sp1 transactivity. We also found that this inhibition of Sp1 transactivity by AML1-ETO is achieved by interaction between Sp1 and RUNT domain of AML1 |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |