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JUN — PDCD11

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
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
Zhu et al., Int J Biochem Cell Biol 2012 (Bone Resorption) : The RANKL stimulated mRNA expression of osteoclast related genes and transcription factors were also diminished by ISL. Mechanistically, ISL blocked the RANKL triggered RANK-TRAF6 association, phosphorylation of mitogen activated protein kinases ( MAPKs ), inhibitor of ?Ba ( I?Ba ) phosphorylation and degradation, nuclear factor-?B ( NF-?B ) p65 nuclear translocation, as well as activator protein (AP)-1 activation
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