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EPX — JUN

Text-mined interactions from Literome

McElhinney et al., J Leukoc Biol 2003 : EPO with substrates induced rapid and sustained activation of c-Jun-NH2-terminal kinase (JNK) and led to cell death, as was evidenced by enhanced mitochondrial depolarization, cytochrome c release, cleavage of caspases 9 and 3, poly-adenosine 5'-diphosphate ribosylation of proteins, the formation of single stranded DNA, and membrane permeability
Jacobs-Helber et al., Blood 2004 : EPO activates Jun N-terminal kinase (JNK) , a member of the mitogen activated protein kinase ( MAPK ) family in the EPO dependent murine erythroid HCD57 cells
Rui et al., Cardiovasc Res 2005 (Myocardial Reperfusion Injury) : An inhibitor of phosphatidylinostol 3 (PI3)-kinase prevented the nuclear translocation of AP-1 induced by EPO
Gewirtz et al., Clin Cancer Res 2006 (Breast Neoplasms...) : EPO stimulated the activation of extracellular signal regulated kinase, p38, and c-Jun-NH ( 2 ) -kinase in MCF-7 cells but did not activate Akt or signal transducers and activators of transcription 5 ( STAT5 )
Patel et al., Exp Hematol 1995 (Second Messenger Systems) : We now report that Epo strongly increases the activity of the transcription factor AP1 in both transformed and normal erythroid cells ... Our results suggest that Epo may induce AP1 activity via a co- or posttranslational mechanism, presumably through modification of the Fos and/or Jun proteins