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data indicated that miR-139-5p was down-regulated in the hearts of Hypertrophic cardiomyopathy patients and that it inhibited cardiac hypertrophy by targetting c-Jun expression.
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this study identified an essential Jun/miR-22/HuR regulatory axis in CRC (the working model is summarised in Fig. 8) and highlighted the vital role of HuR and miR-22 in CRC proliferation and migration.
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a novel cascade mediated by AP-1 and FOXF1 that regulates oncogene-induced senescence, is reported.
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Multivalent Interactions with Fbw7 and Pin1 Facilitate Recognition of c-Jun by the Fbw7.
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High AP-1 expression is associated with metastasis in colon cancer.
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Our results suggest that extended AP-1 binding sites, together with adjacent binding sites for additional TFs, encode part of the information that governs transcription factor binding sites activity in the genome.
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the expression of WIF-1 was low in GBC cells due to aberrant hypermethylation of its promoter region. Additionally, an alternative pathogenesis of GBC was indicated in which c-Jun causes hypermethylation of the WIF-1 promoter region, and represses the expression of WIF-1 through transcriptional regulation and interaction with DNMT1 as an early event in the tumorigenesis of GBC.
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Mutant cellular AP-1 proteins promote expression of a subset of Epstein-Barr virus late genes in the absence of lytic viral DNA replication.
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Secreted Ta9 has therefore, not only the ability to stimulate CD8+ T cells, but also the potential to activate AP-1-driven transcription and contribute to T. annulata-induced leukocyte transformation
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MiR-216b directly targets c-Jun, thereby reducing AP-1-dependent transcription and sensitizing cells to ER stress-dependent apoptosis.
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results suggest that c-Jun, p38 MAPK, PIK3CA/Akt, and GSK3 signaling involved in the effect of miR-203 on the proliferation of hepatocellular carcinoma cells.
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These findings suggest that increased JUN expression and activity may contribute to gefitinib resistance in non-small cell lung cancer.
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the results indicated that butein has antiproliferative and proapoptotic properties through the suppression of NF-kappaB, AP-1 and Akt signaling in HTLV-1-infected T cells, both in vitro and in vivo, suggesting its therapeutic potential against HTLV-1-associated diseases including adult T-cell leukemia/lymphoma
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Results show that VEGFA induces c-jun expression in mediating human retinal microvascular endothelial cell migration, sprouting and tube formation, and that Pyk2-STAT3 signaling enhances cJun expression in the mediation of retinal neovascularization.
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Increased c-jun expression is associated with nasopharyngeal carcinoma.
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thrombin binding to PAR-1 receptor activated Gi-protein/c-Src/Pyk2/EGFR/PI3K/Akt/p42/p44 MAPK cascade, which in turn elicited AP-1 activation and ultimately evoked MMP-9 expression and cell migration in SK-N-SH cells.
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Findings provide evidence that phospho-c-Jun activates an important regulatory mechanism to control DNMT1 expression and regulate global DNA methylation in glioblastoma.
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results demonstrated for the first time the regulatory mechanism of miR-744 transcription by c-Jun, providing a potential mechanism underlying the upregulation of miR-744 in cancers
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Results provide evidence that NuRD represses c-Jun transcription directly which, in the absence of MBD3, activates endogenous pluripotent genes and regulates induced cancer stem cells-related genes.
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Taken together, these results indicated that PAR1 signalingmediated cJun activation promotes early apoptosis of HUVEC cells induced by heat stress.
