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JUN — MYLIP

Text-mined interactions from Literome

Talotta et al., Oncogene 2009 (Cell Transformation, Neoplastic) : Here, we show that the miRNA miR-21 , which represents the most frequently upregulated oncomir in solid tumors, is induced by AP-1 in response to RAS
Tili et al., Carcinogenesis 2010 : We further establish that the downregulation of AP-1 activity by resveratrol is miR-663 dependent and that the effects of resveratrol on both AP-1 activity and JunB levels are dose dependent
Dai et al., Hum Reprod 2011 (Pre-Eclampsia) : DNA precipitation assays and luciferase reporter analysis were used to evaluate the regulation of miR-155 by AP-1 and NF-?B ... Both JunB/FosB and p65 were increased in placenta from women with severe pre-eclampsia versus a normal pregnancy, with elevated expression of miR-155 ( P < 0.05 )
Zhou et al., Proc Natl Acad Sci U S A 2011 (Inflammation) : Overexpression of PPARa significantly attenuated the AP-1 mediated miR-21 expression ... These results demonstrate a unique mechanism by which OSS induces AP-1 dependent miR-21 expression, which directly targets PPARa to inhibit its expression, thereby allowing activation of AP-1 and the promotion of monocyte adhesion
Acunzo et al., Oncogene 2012 (Carcinoma, Non-Small-Cell Lung...) : Here, we further investigated this pathway and showed that miR-130a, expressed at low level in lung cancer cell lines, by targeting MET was able to reduce TRAIL resistance in NSCLC cells through the c-Jun mediated downregulation of miR-221 and miR-222
Arora et al., PloS one 2011 (Lung Neoplasms) : When c-Jun N-terminal kinase activity was inhibited using SP600125, expression of miR-26b was induced following ?-irradiation in H1299 cells
Zhou et al., PloS one 2012 : In addition, we found that miR-222 might regulate the phosphorylation of cAMP response element binding protein ( CREB ) through PTEN, and c-Jun activation might enhance the miR-222 expression
Song et al., PloS one 2012 : Stretch upregulates miR-21 expression at least in part at the transcription level and AP-1 is essential for stretch induced miR-21 expression
Shen et al., PloS one 2013 (Cell Transformation, Neoplastic) : Down-regulation of miR-21 and up-regulations of Pdcd44 or Spry1 blocked the arsenite induced activations of JNK/c-Jun or ERK/NF-?B, indicating that knockdown of miR-21 inhibits feedback of ERK activation and JNK activation via increases of Pdcd4 and Spry1 protein levels, respectively
Cheng et al., J Biol Chem 2013 (Alzheimer Disease) : Moreover, we also showed that activator protein-1 regulates the transcription of miR-144 and the up-regulation of miR-144 at least partially induces the suppression of the ADAM10 protein in the presence of Aß
Sonkoly et al., Oncogenesis 2012 : We identify c-JUN , a key effector of the HH pathway, as a novel direct target for miR-203 in vivo
Yu et al., Cell death & disease 2013 (Cell Transformation, Neoplastic...) : Further, we discovered that attenuated CTGF mediated upregulation of miR-18b was dependent on the increased binding of transcription factors Jun proto-oncogene (C-Jun) and v-Myc myelocytomatosis viral oncogene homolog ( C-Myc ) to miR-18b promoter region via phosphoinositide 3-kinase (PI3K)/AKT pathway ... Our studies are the first to demonstrate that reduced CTGF as an unfavorable prognosis factor mediates the activation of miR-18b , an oncomir directly suppresses CTGF expression, by PI3K/AKT/C-Jun and C-Myc and promotes cell growth of NPC
Onyeagucha et al., Exp Cell Res 2013 (Colonic Neoplasms) : Altogether, these data demonstrate that the expression of miR-155 is regulated by S100P and is dependent on RAGE activation and stimulation of AP-1
Yang et al., PloS one 2013 (Carcinoma, Hepatocellular...) : In turn, TGFß decreases miR-127 expression by enhancing c-Jun mediated inhibition of miR-127 promoter activity
Kang et al., Mol Biol Rep 2013 : miR-21 could significantly promote adipocyte differentiation, increase adiponectin mRNA and protein expression, while decrease AP-1 protein level