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HPR — JUN

Text-mined interactions from Literome

Chen et al., Mol Pharmacol 1999 : 4-HPR caused sustained c-Jun N-terminal kinase (JNK) activation and apoptosis in LNCaP cells but not in PC-3 cells at the dosages tested
Um et al., Biol Pharm Bull 2003 (Ovarian Neoplasms) : However, like natural retinoids, 4-HPR and compound 3 actively suppressed c-Jun transcriptional activity
Appierto et al., Cell Death Differ 2004 (Carcinoma...) : In gene reporter experiments, HPR stimulated AP-1 transcriptional activity and potentiated the AP-1 activity induced by 12-tetradecanoylphorbol 13-acetate
Darwiche et al., Radiat Res 2005 (Skin Neoplasms) : Interestingly, pretreatments with tRA and cRA, but not HPR , suppressed UVB-radiation induced AP1 activity by more than 50 %, whereas post-treatment failed to produce similar effects
Kim et al., Int J Oncol 2005 (Carcinoma, Squamous Cell...) : The increase in the level of p67phox protein may be a downstream effect of the activation of c-Jun N-terminal kinase (JNK) induced by 4HPR
Kim et al., Oncogene 2006 (Carcinoma, Squamous Cell...) : 4HPR induced activation of these kinases was abrogated by the antioxidants BHA and vitamin C. SP600125, a JNK inhibitor, suppressed 4HPR induced c-Jun phosphorylation, cytochrome c release from mitochondria and apoptosis