◀ Back to JUN

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