-
results suggested that four differentially expressed genes, Jun, Gal, Cd74, and C1qb, had the potential to serve as prognostic or predictive markers for neuropathic pain, suggesting a potential application in the improvement of prognostic tools and treatments.
-
High expression of c-Jun or Fra-1 was associated with poor prognosis in oral squamous cell carcinoma patients.
-
High c-Jun expression is associated with oral squamous cell carcinoma.
-
the present study demonstrated that the AP-1 complex may be a novel regulator of MANF transcriptional enhancement, and that MANF is a novel downstream target of AP-1, which may indicate a novel role of AP-1 in regulating inflammatory pathways.
-
USP6 is an enzyme that deubiquitinates c-Jun and regulates its downstream cellular functions.USP6 regulates the stability of the c-Jun protein in an enzyme activity-dependent manner.
-
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.
-
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.
-
a novel cascade mediated by AP-1 and FOXF1 that regulates oncogene-induced senescence, is reported.
-
Multivalent Interactions with Fbw7 and Pin1 Facilitate Recognition of c-Jun by the Fbw7.
-
High AP-1 expression is associated with metastasis in colon cancer.
-
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.
-
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.
-
Mutant cellular AP-1 proteins promote expression of a subset of Epstein-Barr virus late genes in the absence of lytic viral DNA replication.
-
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
-
MiR-216b directly targets c-Jun, thereby reducing AP-1-dependent transcription and sensitizing cells to ER stress-dependent apoptosis.
-
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.
-
These findings suggest that increased JUN expression and activity may contribute to gefitinib resistance in non-small cell lung cancer.
-
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
-
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.
-
Increased c-jun expression is associated with nasopharyngeal carcinoma.
