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JUN — PDCD4
Text-mined interactions from Literome
Grimm et al., Cell Death Differ 2001
(Vision, Ocular) :
Here we show that N-terminal phosphorylation of
c-Jun , the other main partner of c-Fos in induced AP-1 complexes is not
required for
programmed cell death during retinal development in vivo and is also dispensable for photoreceptor apoptosis induced by the exogenous stimuli `` excessive light '' and N-nitroso-N-methylurea ( MNU )
Lehmann et al., Cell Death Differ 2002
:
This study demonstrates a
role for
AP-1 in the stage-specific steroid triggered
programmed cell death of larval tissues during Drosophila metamorphosis
Jansen et al., Cancer Res 2005
(Carcinoma, Squamous Cell...) :
These results extend to an in vivo model the observations that
Pdcd4 inhibits both translation initiation and
AP-1 activation while decreasing benign tumor development and malignant progression
Palamarchuk et al., Cancer Res 2005
:
Using luciferase assay, we show that phosphorylation of
Pdcd4 by Akt also
causes a significant decrease of the ability of Pdcd4 to interfere with the transactivation of
AP-1-responsive promoter by c-Jun
Talotta et al., Oncogene 2009
(Cell Transformation, Neoplastic) :
We further show that, given the role of PDCD4 as negative regulator of AP-1, the miR-21 mediated downregulation of
PDCD4 is
essential for the maximal induction of
AP-1 activity in response to RAS
Inuzuka et al., Nature 2011
(Precursor T-Cell Lymphoblastic Leukemia-Lymphoma) :
In addition to accelerating cell growth, overexpression of
Jun , Myc or notch 1 can also
induce programmed cell death
Marti et al., Oncogene 1994
:
A similar induction of AP-1 ( cFos/JunD ) was also observed in the involuting rat ventral prostate pointing to a possible
role for
AP-1 in
programmed cell death
Xu et al., Proc Natl Acad Sci U S A 1997
:
Activation of the recently identified
c-Jun N-terminal kinases (JNKs) typically
results in
programmed cell death ( apoptosis ) in neurons and other cell types grown in culture