◀ Back to HDAC2
HDAC2 — RUNX1
Pathways - manually collected, often from reviews:
-
KEGG Pathways in cancer:
MECOM/RUNX1
→
Complex of CTBP1-CTBP2-HDAC1-HDAC2
(protein-protein, activation)
-
KEGG Chronic myeloid leukemia:
MECOM/RUNX1
→
Complex of CTBP1-CTBP2-HDAC1-HDAC2
(protein-protein, activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Izutsu et al., Oncogene 2002
(Leukemia, Myeloid) :
Here, we demonstrate that AML1/Evi-1 interacts with CtBP in SKH1 cells, a leukemic cell line which endogenously overexpresses AML1/Evi-1 and that
AML1/Evi-1 requires the interaction with
CtBP to repress AML1 induced transactivation
Imai et al., Mol Cell Biol 2004
:
The corepressor
mSin3A regulates phosphorylation induced activation, intranuclear location, and stability of
AML1 ... Here, we demonstrate that the interaction between AML1 and the corepressor
mSin3A is regulated by phosphorylation of AML1 and that release of
AML1 from mSin3A
induced by phosphorylation activates its transcriptional activity
Chan et al., Blood 2005
(Myelodysplastic Syndromes...) :
These results suggest a central
role for
CtBP in
AML1-FOG2 transcriptional repression and implicate coordinated disruption of the AML1 and GATAdevelopmental programs in the pathogenesis of myelodysplasia
Takahashi et al., Br J Haematol 2005
(Acute Disease...) :
We verified that the repression activity of
AML1B , the isoform of AML1, is
dependent on
HDAC activity by using HDAC inbitor trichostatin A in GAL4 reporter assays
Lutterbach et al., Mol Cell Biol 1998
(Leukemia, Myeloid...) :
Finally,
AML-1/ETO associates with histone deacetylase activity and a
histone deacetylase inhibitor
impairs the ability of the fusion protein to repress transcription