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JUN — RUNX1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Frank et al., Oncogene 1999
(Cell Transformation, Neoplastic...) :
Expression of
AML1/ETO increased the level of
c-Jun-P ( ser63 ), and activated AP-1 dependent transcription, which was inhibited by expression of a dominant negative c-Jun protein
Elsässer et al., Oncogene 2003
(Leukemia, Myeloid, Acute...) :
These data suggest a model in which
AML1-ETO induces
proto-oncogene c-jun expression via the proximal AP-1 site of the c-jun promoter in a JNK dependent manner
Mitani et al., Oncogene 2004
(Leukemia) :
Lastly,
AML1/EVI-1 enhances
AP-1 activity by activating the c-Fos promoter depending on the second zinc-finger domain of EVI-1, and promotes cell proliferation
Bowers et al., Nucleic Acids Res 2010
:
Furthermore, we demonstrated that binding of
Runx1 to the enhancer is rigidly controlled at the level of chromatin accessibility, and is
dependent upon prior induction of NFAT and
AP-1 , which disrupt a positioned nucleosome in this region
Kurokawa et al., Oncogene 1995
(Cell Transformation, Neoplastic...) :
We showed that the transforming effect is correlated with the
AP-1 activation
induced by
AML1/Evi-1
Tanaka et al., Mol Cell Biol 1995
(Cell Transformation, Neoplastic...) :
Furthermore,
AML1/Evi-1 stimulated c-fos promoter transactivation and increased
AP-1 activity, as Evi-1 ( which is not normally expressed in hemopoietic cells ) did